Hypersensitivity Reactions Overview
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Questions and Answers

What is a primary requirement for an individual to have a hypersensitivity reaction to an antigen?

  • Presence of susceptibility genes
  • Previous sensitization to the antigen (correct)
  • Presence of IgG antibodies
  • Exposure to the antigen for the first time

    • Which statement accurately describes Type I hypersensitivity reactions?

  • They are predominantly mediated by IgG antibodies.
  • They involve mast cell degranulation triggered by IgE antibodies. (correct)
  • They usually occur over a period of hours after allergen exposure.
  • They represent a chronic immune response.

    • Which of the following is NOT a characteristic of Type I hypersensitivity reactions?

  • Occurs in 10-20% of the population.
  • Produces immediate allergic reactions.
  • Mediated by IgE antibodies.
  • Symptoms appear after several hours of exposure. (correct)

    • What is the origin of exogenous antigens in hypersensitivity reactions?

    <p>Derived from external sources</p> Signup and view all the answers

    Which type of hypersensitivity reaction is characterized by immune complex-mediated disorders?

    <p>Type III hypersensitivity</p> Signup and view all the answers

    How is genetic susceptibility related to hypersensitivity reactions?

    <p>It involves the inheritance of certain susceptibility genes.</p> Signup and view all the answers

    What defines the time frame of an immediate hypersensitivity reaction?

    <p>Occurs within 5-10 minutes</p> Signup and view all the answers

    Which cells are primarily involved in the mechanism of Type I hypersensitivity?

    <p>Mast cells</p> Signup and view all the answers

    What is a characteristic feature of the late-phase reaction in type I hypersensitivity?

    <p>Infiltration of eosinophils</p> Signup and view all the answers

    Which of the following is NOT typically a feature of anaphylactic shock?

    <p>Increased mucus secretion</p> Signup and view all the answers

    What type of antibodies are primarily involved in type II hypersensitivity reactions?

    <p>IgG</p> Signup and view all the answers

    What is a common precursor to allergic conditions such as hay fever and asthma?

    <p>Atopic eczema</p> Signup and view all the answers

    What happens during the sensitization phase when an allergen is first encountered?

    <p>T cells differentiate into TH2 cells after antigen presentation.</p> Signup and view all the answers

    What role do prostaglandins play in the late-phase reaction of type I hypersensitivity?

    <p>Tissue infiltration</p> Signup and view all the answers

    Which cytokine is primarily responsible for stimulating B cells to produce IgE antibodies during sensitization?

    <p>IL-4</p> Signup and view all the answers

    What is the main effector cell involved in type I hypersensitivity reactions?

    <p>Mast cells</p> Signup and view all the answers

    Which of the following substances predominantly causes cell lysis in type II hypersensitivity reactions?

    <p>Antibodies</p> Signup and view all the answers

    During the immediate phase response of an allergic reaction, which of the following mediators is released from mast cells?

    <p>Histamine</p> Signup and view all the answers

    Which of the following cells is NOT involved in the inflammatory response during type I hypersensitivity?

    <p>T-helper 1 cells</p> Signup and view all the answers

    Which of the following best describes the mechanism of antibody-dependent cellular cytotoxicity in type II hypersensitivity?

    <p>Antibody binding leading to cell death via complement</p> Signup and view all the answers

    Which of the following accurately describes the re-exposure to an allergen in individuals with atopy?

    <p>Mast cells and basophils undergo activation and degranulation.</p> Signup and view all the answers

    What is the expected time frame for the immediate phase response to occur after exposure to an allergen?

    <p>Within 5 to 30 minutes</p> Signup and view all the answers

    Which statement about mast cells in type I hypersensitivity is incorrect?

    <p>Mast cells are only present in the bloodstream.</p> Signup and view all the answers

    What role do eosinophils play during the hypersensitivity response?

    <p>Being activated by IL-5 during the sensitization phase</p> Signup and view all the answers

    What is the primary mechanism of injury in transfusion reactions due to ABO or Rh incompatibility?

    <p>Direct lysis through complement activation</p> Signup and view all the answers

    In the context of type II hypersensitivity, which of the following describes opsonization?

    <p>Coating of cells with antibodies to enhance phagocytosis</p> Signup and view all the answers

    Which condition is characterized by antibodies that stimulate the thyroid leading to hyperthyroidism?

    <p>Grave’s disease</p> Signup and view all the answers

    What is a common feature shared by conditions such as autoimmune hemolytic anemia and idiopathic thrombocytopenic purpura (ITP)?

    <p>Both involve destruction of blood cells via antibodies</p> Signup and view all the answers

    Which mechanism describes the process when antibodies bind to target cells but do not induce phagocytosis?

    <p>Antibody-dependent cellular cytotoxicity</p> Signup and view all the answers

    In type II hypersensitivity reactions, what occurs when autoantibodies coat red blood cells after penicillin administration?

    <p>Triggers phagocytosis by macrophages</p> Signup and view all the answers

    In Hashimoto thyroiditis, the antibodies primarily affect which aspect of thyroid function?

    <p>Block the action of thyroid-stimulating hormone (TSH)</p> Signup and view all the answers

    Which of the following is NOT an example of a type II hypersensitivity reaction?

    <p>Anaphylactic shock</p> Signup and view all the answers

    Type I hypersensitivity reactions occur within 30-40 minutes after antigen exposure.

    <p>False</p> Signup and view all the answers

    Exogenous antigens can include substances like drugs and dust.

    <p>True</p> Signup and view all the answers

    Hypersensitivity reactions are solely due to environmental allergens.

    <p>False</p> Signup and view all the answers

    Individuals with immediate hypersensitivity reactions exhibit low levels of serum IgE.

    <p>False</p> Signup and view all the answers

    Genetic susceptibility plays no role in the development of hypersensitivity disorders.

    <p>False</p> Signup and view all the answers

    Type II hypersensitivity is characterized by the involvement of IgE antibodies and mast cells.

    <p>False</p> Signup and view all the answers

    Sensitization to an allergen requires prior exposure to that allergen.

    <p>True</p> Signup and view all the answers

    Type III hypersensitivity reactions are exclusively triggered by self-antigens.

    <p>False</p> Signup and view all the answers

    Individuals who are genetically susceptible to allergens are termed atopic.

    <p>True</p> Signup and view all the answers

    The immediate phase response of an allergic reaction begins 30 to 60 minutes after exposure to an allergen.

    <p>False</p> Signup and view all the answers

    Mast cells are concentrated primarily near blood vessels and nerves and play a key role in type I hypersensitivity reactions.

    <p>True</p> Signup and view all the answers

    During the sensitization phase, IgE antibodies are produced to mediate the response upon re-exposure to the antigen.

    <p>True</p> Signup and view all the answers

    IL-5 secreted by TH2 cells is responsible for stimulating B cells to secrete IgE antibodies.

    <p>False</p> Signup and view all the answers

    Histamine is one of the mediators released by mast cells during the degranulation process upon re-exposure to an allergen.

    <p>True</p> Signup and view all the answers

    The degranulation of mast cells occurs immediately upon first exposure to an allergen.

    <p>False</p> Signup and view all the answers

    Smooth muscle contraction is a feature of the immediate phase response in type I hypersensitivity.

    <p>True</p> Signup and view all the answers

    The late-phase reaction of type I hypersensitivity is characterized by the release of histamine and immediate vascular leakage.

    <p>False</p> Signup and view all the answers

    Anaphylactic shock can occur after the injection of drugs like penicillin in sensitive patients.

    <p>True</p> Signup and view all the answers

    Eosinophils, neutrophils, and basophils are primarily involved in the immediate phase of type I hypersensitivity.

    <p>False</p> Signup and view all the answers

    Antibodies involved in type II hypersensitivity reactions are predominantly IgE and IgA.

    <p>False</p> Signup and view all the answers

    Systemic allergic reactions can lead to symptoms like urticaria and dyspnea.

    <p>True</p> Signup and view all the answers

    Prostaglandins are associated with the immediate phase of allergic reactions, causing rapid mucosal damage.

    <p>False</p> Signup and view all the answers

    The presence of eosinophils in tissue samples is an indicator of chronic inflammation in type I hypersensitivity.

    <p>True</p> Signup and view all the answers

    Antibody-mediated cellular dysfunction occurs when antibodies induce phagocytosis of target cells.

    <p>False</p> Signup and view all the answers

    Incompatible blood transfusion leads to cell lysis due to complement activation.

    <p>True</p> Signup and view all the answers

    Phagocytosis can occur without antibodies binding to the target cells.

    <p>False</p> Signup and view all the answers

    Antibody dependent cellular cytotoxicity operates through perforin and granzyme without cell phagocytosis.

    <p>True</p> Signup and view all the answers

    In Grave's disease, antibodies block the TSH receptors on thyroid cells.

    <p>False</p> Signup and view all the answers

    Autoimmune hemolytic anemia is an example of type II hypersensitivity.

    <p>True</p> Signup and view all the answers

    Opsonization refers to the process where antibodies coat pathogens making them less visible to immune cells.

    <p>False</p> Signup and view all the answers

    The mechanism responsible for hemolytic disease of the newborn is related to type I hypersensitivity.

    <p>False</p> Signup and view all the answers

    In antibody-mediated cellular dysfunction, antibodies can either activate or block cellular functions.

    <p>True</p> Signup and view all the answers

    Explain the dual role of genetic susceptibility and environmental exposure in hypersensitivity reactions.

    <p>Genetic susceptibility predisposes individuals to hypersensitivity reactions, while environmental exposure provides the necessary antigens for the immune system to respond to.</p> Signup and view all the answers

    Describe the mechanism that leads to the rapid response observed in Type I hypersensitivity reactions.

    <p>Type I hypersensitivity reactions occur when allergens bind to IgE antibodies on mast cells, triggering degranulation and the immediate release of inflammatory mediators like histamine.</p> Signup and view all the answers

    What distinguishes exogenous antigens from endogenous antigens in the context of hypersensitivity reactions?

    <p>Exogenous antigens originate from outside the body, such as pollen and dust, while endogenous antigens are derived from the individual's own tissues.</p> Signup and view all the answers

    Identify the type of antibody primarily involved in type II hypersensitivity and its role.

    <p>IgG and IgM antibodies are primarily involved in type II hypersensitivity, as they mediate opsonization and promote phagocytosis of target cells.</p> Signup and view all the answers

    What role do mast cells play in the development of anaphylactic reactions during Type I hypersensitivity?

    <p>Mast cells store and release histamine and other inflammatory mediators upon re-exposure to an allergen, contributing significantly to anaphylactic reactions.</p> Signup and view all the answers

    How does sensitization to an allergen affect subsequent immune responses in atopic individuals?

    <p>Sensitization leads to the production of IgE antibodies that bind to mast cells, priming the immune system for a heightened response upon re-exposure.</p> Signup and view all the answers

    Discuss the concept of hypersensitivity as a pathological response and its potential outcomes.

    <p>Hypersensitivity is an exaggerated immune response that can result in tissue injury, autoimmune diseases, or allergic reactions, sometimes leading to fatal outcomes.</p> Signup and view all the answers

    What is the significance of the sensitization phase in the context of allergic reactions?

    <p>The sensitization phase is crucial as it establishes the immune memory by producing IgE antibodies in response to an allergen, enabling a more vigorous reaction upon subsequent exposures.</p> Signup and view all the answers

    What are the roles of TH2 cells and IL-4 in type I hypersensitivity during the sensitization phase?

    <p>TH2 cells secrete IL-4, which stimulates B cells to produce IgE antibodies essential for sensitization.</p> Signup and view all the answers

    Explain the difference between the primary and secondary immune responses in atopic individuals upon allergen re-exposure.

    <p>During primary exposure, no reaction occurs as sensitization develops; upon secondary exposure, cross-linking of IgE triggers rapid mast cell degranulation.</p> Signup and view all the answers

    Describe the role of eosinophils in type I hypersensitivity after sensitization.

    <p>Eosinophils are activated by IL-5 secreted from TH2 cells and contribute to inflammation and tissue damage during allergic responses.</p> Signup and view all the answers

    What are the mediators released during the immediate phase response of type I hypersensitivity, and what is their impact?

    <p>Mediators such as histamine and leukotrienes cause vasodilation, increased permeability, and smooth muscle contraction, leading to allergy symptoms.</p> Signup and view all the answers

    What is the significance of mast cell sensitization via IgE antibodies in type I hypersensitivity reactions?

    <p>Mast cell sensitization via IgE antibodies allows for rapid response during re-exposure to allergens, triggering degranulation.</p> Signup and view all the answers

    In type I hypersensitivity, how does the timing of the immediate phase response influence the symptoms experienced by an individual?

    <p>The immediate phase response occurs within 5 to 30 minutes, leading to sudden onset symptoms like wheezing and hives.</p> Signup and view all the answers

    How does genetic susceptibility affect the development of type I hypersensitivity among individuals?

    <p>Genetic susceptibility predisposes individuals to develop atopy, where they are more likely to produce IgE against harmless allergens.</p> Signup and view all the answers

    What is the timeline of events encountered during the re-exposure to an allergen in sensitized individuals?

    <p>Upon re-exposure, the allergen cross-links IgE on mast cells, leading to degranulation and the rapid release of inflammatory mediators.</p> Signup and view all the answers

    What are the main features of the late-phase reaction following exposure to an allergen in type I hypersensitivity?

    <p>The late-phase reaction involves the release of secondary mediators from mast cells, including prostaglandins and leukotrienes, and is characterized by eosinophil infiltration and mucosal epithelial cell damage.</p> Signup and view all the answers

    Explain the significance of eosinophils in type I hypersensitivity reactions.

    <p>Eosinophils play a crucial role in the late-phase response by infiltrating tissues, contributing to inflammation and tissue damage associated with allergic reactions.</p> Signup and view all the answers

    Describe the pathophysiological mechanisms causing anaphylactic shock in type I hypersensitivity reactions.

    <p>Anaphylactic shock occurs due to a rapid release of mediators from mast cells, leading to widespread vasodilation, hypotension, and increased vascular permeability.</p> Signup and view all the answers

    Identify the primary immunological components involved in type II hypersensitivity reactions.

    <p>Type II hypersensitivity primarily involves IgG and IgM antibodies that bind to antigens on cell surfaces, leading to cell lysis and damage.</p> Signup and view all the answers

    What role do prostaglandins play in the immune response during the late-phase reaction of type I hypersensitivity?

    <p>Prostaglandins contribute to inflammation by causing vasodilation and increased vascular permeability, further exacerbating the allergic response.</p> Signup and view all the answers

    How do antibody-mediated cellular dysfunctions manifest in type II hypersensitivity reactions?

    <p>Antibody-mediated cellular dysfunction can lead to altered cellular functions without necessarily causing cell lysis, such as in conditions like myasthenia gravis.</p> Signup and view all the answers

    What distinguishes immediate hypersensitivity reactions from late-phase reactions?

    <p>Immediate hypersensitivity reactions occur within minutes due to the rapid release of preformed mediators, while late-phase reactions develop hours later through ongoing inflammation.</p> Signup and view all the answers

    Provide an example of an exogenous antigen in type II hypersensitivity and its effects.

    <p>Penicillin can act as an exogenous antigen by binding to red blood cells and inducing an immune response that leads to hemolytic anemia.</p> Signup and view all the answers

    Explain the role of C3b and antibodies in the mechanism of cell lysis.

    <p>C3b binds to the target cell along with antibodies like IgG and IgM, activating the complement system to cause cell lysis.</p> Signup and view all the answers

    How does opsonization facilitate phagocytosis in autoimmune hemolytic anemia?

    <p>In autoimmune hemolytic anemia, autoantibodies coat erythrocytes, marking them for phagocytosis by macrophages.</p> Signup and view all the answers

    What distinguishes antibody-dependent cellular cytotoxicity from traditional phagocytosis?

    <p>Antibody-dependent cellular cytotoxicity involves natural killer cells or macrophages linking to target cells without engulfing them.</p> Signup and view all the answers

    In the context of Type II hypersensitivity, what is the impact of antibodies on tissue receptor function?

    <p>Antibodies can block or misregulate receptor function, causing conditions such as Hashimoto's thyroiditis or Graves' disease.</p> Signup and view all the answers

    Identify a condition where antibodies against the TSH receptor lead to hyperthyroidism.

    <p>Graves' disease occurs when antibodies stimulate the TSH receptor, resulting in excessive thyroid hormone production.</p> Signup and view all the answers

    What is the primary mechanism that leads to hemolytic disease of the newborn?

    <p>Hemolytic disease of the newborn occurs when maternal antibodies cross the placenta and attack fetal red blood cells.</p> Signup and view all the answers

    Describe how drug-induced cytotoxic antibodies can lead to platelet destruction.

    <p>Drugs can modify platelets, prompting the immune system to produce antibodies that mark them for destruction.</p> Signup and view all the answers

    What role does phagocytosis play in the context of penicillin-induced hemolytic anemia?

    <p>Penicillin-induced hemolytic anemia involves macrophages phagocytosing red blood cells coated with IgG antibodies against penicillin.</p> Signup and view all the answers

    Match the following components with their roles in Type I hypersensitivity:

    <p>IgE Antibodies = Bind to mast cells and basophils TH2 Cells = Secrete cytokines like IL-4 and IL-5 Mast Cells = Release mediators upon re-exposure to allergen Eosinophils = Activated by IL-5 to mediate inflammatory response</p> Signup and view all the answers

    Match the following phases of hypersensitivity response with their descriptions:

    <p>Sensitization Phase = Initial exposure leads to IgE production Immediate Phase = Reaction occurs within 5 to 30 minutes Late Phase = Prolonged response with additional mediators Degranulation = Mast cells release histamine and cytokines</p> Signup and view all the answers

    Match the following cytokines with their functions in Type I hypersensitivity:

    <p>IL-4 = Stimulates B cells to produce IgE antibodies IL-5 = Activates eosinophils for tissue infiltration IL-13 = Stimulates mucus secretion from epithelial cells Histamine = Causes vasodilation and increased permeability</p> Signup and view all the answers

    Match the following immune cells with their characteristics:

    <p>Mast Cells = Contain Fc receptors for IgE binding Basophils = Release mediators during allergic reactions B Cells = Produce specific antibodies like IgE during sensitization T Cells = Differentiate into TH2 cells in response to antigens</p> Signup and view all the answers

    Match the following allergens with their common sources:

    <p>House-dust mite = Common indoor allergen Pollens = Seasonal outdoor allergen Animal danders = Pet-related allergen Moulds = Fungal allergen present in damp environments</p> Signup and view all the answers

    Match the following types of hypersensitivity with their definitions:

    <p>Type I = IgE-mediated immediate hypersensitivity Type II = Cytotoxic hypersensitivity involving IgG or IgM Type III = Immune complex-mediated reactions Type IV = Delayed-type hypersensitivity mediated by T cells</p> Signup and view all the answers

    Match the following terms with their corresponding phases of an allergic reaction:

    <p>Degranulation = Release of pre-formed mediators from mast cells Cytokine release = Occurs after activation of TH2 cells Immediate hypersensitivity = Rapid reaction upon second exposure Late-phase response = Involves recruitment of additional immune cells</p> Signup and view all the answers

    Match the following characteristics with their respective type of hypersensitivity reaction:

    <p>Immediate-phase reaction = Vasodilation and smooth muscle spasm Late-phase reaction = Infiltration with eosinophils and TH2 cells Localized type I HSR = Hay fever and asthma Systemic type I HSR = Anaphylactic shock and hypotension</p> Signup and view all the answers

    Match the following statements with their respective components of immune response:

    <p>Fc receptor = High affinity for IgE antibodies on mast cells Epithelial cells = Stimulated by IL-13 to secrete mucus Cytokines = Mediators released by activated TH2 cells IgE sensitization = Initiates the allergic response upon re-exposure</p> Signup and view all the answers

    Match the mediators released during type I hypersensitivity reactions with their effects:

    <p>Histamine = Increased vascular permeability Prostaglandins = Mucosal epithelial cell damage Leukotrienes = Bronchospasm Cytokines = Recruitment of leukocytes</p> Signup and view all the answers

    Match the type II hypersensitivity mechanism with its description:

    <p>Complement dependent HSR = Opsonization and phagocytosis Antibody dependent cellular cytotoxicity = Direct lysis of target cells Antibody mediated cellular dysfunction = Altered cell function without lysis IgG and IgM antibodies = Primary antibodies involved in type II reactions</p> Signup and view all the answers

    Match the examples with their respective type of hypersensitivity reaction:

    <p>Autoimmune hemolytic anemia = Type II hypersensitivity Hay fever = Type I hypersensitivity Anaphylaxis = Systemic type I hypersensitivity Extrinsic asthma = Localized type I hypersensitivity</p> Signup and view all the answers

    Match the types of cells involved in type I hypersensitivity with their roles:

    <p>Mast cells = Release of mediators like histamine Eosinophils = Inflammatory response and tissue damage Basophils = Histamine release in allergic reactions TH2 cells = Stimulate B cells to produce IgE</p> Signup and view all the answers

    Match the cellular infiltrates with their role in type I late-phase reactions:

    <p>Eosinophils = Tissue inflammation and damage Neutrophils = Acute inflammatory response Basophils = Mediator release Monocytes = Chronic inflammation</p> Signup and view all the answers

    Match the type of antibodies with their roles in hypersensitivity reactions:

    <p>IgE = Mediates type I hypersensitivity IgG = Common in type II hypersensitivity IgM = Rarely involved in type II hypersensitivity IgA = Not primarily involved in hypersensitivity</p> Signup and view all the answers

    Match the symptoms with the corresponding type of hypersensitivity reaction:

    <p>Nasal congestion and sneezing = Localized type I HSR Wheezing and respiratory distress = Bronchial asthma Urticaria and hypotension = Systemic type I HSR Cell lysis and anemia = Type II hypersensitivity</p> Signup and view all the answers

    Match the type of hypersensitivity reaction with its characteristics:

    <p>Type I hypersensitivity = Mediated by IgE antibodies and occurs quickly within 5-10 minutes Type II hypersensitivity = Antibody-mediated, involving tissue-specific antigens Type III hypersensitivity = Involves immune complexes that can deposit in tissues Type IV hypersensitivity = Cell-mediated response that occurs hours to days after exposure</p> Signup and view all the answers

    Match the type of antigen with its origin:

    <p>Exogenous antigens = Green plants or chemicals in the environment Endogenous antigens = Self antigens produced by the body Food allergens = Antigens commonly found in various edibles Drug allergens = Pharmaceutical agents that can trigger hypersensitivity</p> Signup and view all the answers

    Match the characteristic of hypersensitivity with its definition:

    <p>Sensitization = The process of becoming sensitive to an allergen Allergen = A substance that can induce an immune response IgE antibodies = Immunoglobulins primarily involved in allergic reactions Genetic susceptibility = The inherited predisposition to develop hypersensitivity diseases</p> Signup and view all the answers

    Match the feature of type I hypersensitivity with its description:

    <p>Immediate reaction = Occurs within minutes of exposure to an allergen Atopic disorders = Commonly include conditions like asthma and hay fever Elevated serum IgE = A characteristic of individuals with type I hypersensitivity Mast cells = Cells that release histamine during an allergic response</p> Signup and view all the answers

    Match the hypersensitivity type with its mediator:

    <p>Type I = IgE Type II = IgG or IgM Type III = Immune complexes Type IV = T cells</p> Signup and view all the answers

    Match the immune response mechanism with its classification:

    <p>Opsonization = Enhances phagocytosis of antigens by marking them Cytotoxicity = Involves direct killing of target cells by antibodies Immune complex deposition = Leads to inflammation in tissues affected by antigens Delayed-type hypersensitivity = Involves T cell activation and cytokine release</p> Signup and view all the answers

    Match the reaction time frame with the hypersensitivity type:

    <p>Type I = 5-10 minutes Type II = Minutes to hours Type III = Hours to days Type IV = Days to weeks</p> Signup and view all the answers

    Match the following conditions with their associated hypersensitivity type:

    <p>Asthma = Type I Hemolytic anemia = Type II Systemic lupus erythematosus = Type III Contact dermatitis = Type IV</p> Signup and view all the answers

    Match the following mechanisms of injury in Type II hypersensitivity with their descriptions:

    <p>Cell lysis = Antibody-dependent activation of the complement leading to cell destruction. Phagocytosis = Opsonization of cells with antibodies for destruction by macrophages. Antibody-dependent cellular cytotoxicity = Target cells error destroyed by natural killer cells without phagocytosis. Antibody-mediated cellular dysfunction = Antibodies block receptors preventing normal cell function.</p> Signup and view all the answers

    Match the examples of Type II hypersensitivity reactions with their specific conditions:

    <p>Autoimmune haemolytic anemia = Destruction of red blood cells by autoantibodies. Hemolytic disease of the newborn = Maternal antibodies attack fetal red blood cells. Idiopathic thrombocytopenic purpura = Destruction of platelets via autoantibodies. Transfusion reactions = Mismatch of blood types leading to hemolysis.</p> Signup and view all the answers

    Match the antibodies involved in Type II hypersensitivity with their roles:

    <p>IgG = Main antibody involved in opsonization and phagocytosis. IgM = Pentamer that activates complement during cell lysis. IgA = Present in mucosal areas but not directly involved in Type II. IgE = Primarily associated with Type I hypersensitivity but mentioned.</p> Signup and view all the answers

    Match the conditions characterized by antibodies against TSH receptors:

    <p>Hashimoto's thyroiditis = Antibodies block TSH receptor function leading to hypothyroidism. Grave's disease = Antibodies mimic TSH, causing excessive thyroid stimulation. Thyroid storm = Acute condition caused by excessive thyroid hormones. Subclinical hyperthyroidism = Mild elevation in thyroid hormone levels.</p> Signup and view all the answers

    Match the type II hypersensitivity mediators with their actions:

    <p>Complement proteins = Mediate lysis of target cells. Natural killer cells = Destroy target cells by perforin and granzyme. Macrophages = Engulf opsonized cells leading to phagocytosis. Antibodies = Link antigens on cells to immune cells.</p> Signup and view all the answers

    Match the medical conditions with their associated antibody responses:

    <p>Drug-induced cytotoxic antibodies = Antibodies formed against drugs, causing cytotoxicity. Transfusion reaction = Responses against foreign RBC antigen during transfusion. Erythroblastosis foetalis = Maternal antibodies harm fetal RBCs. Incompatible blood transfusion = Immediate hemolysis due to blood type mismatch.</p> Signup and view all the answers

    Match the following antibodies with their roles in Type II hypersensitivity reactions:

    <p>IgG = Commonly involved in opsonization. IgM = Effective in activating the complement cascade. IgD = Primarily a marker of B cell activation. IgA = Mainly found in secretions, not involved in Type II.</p> Signup and view all the answers

    Match the mechanisms leading to blood cell destruction in Type II hypersensitivity:

    <p>Opsonization = Coating of cells with antibodies for phagocytosis. Complement-mediated lysis = Lysis of cells via antibody-activated complement. Antigen-antibody complex formation = Involving antibodies binding to target cell antigens. Direct cellular destruction = Natural killer cells targeting without phagocytosis.</p> Signup and view all the answers

    Study Notes

    Hypersensitivity Reactions

    • A pathological, hyperfunctional, and injurious immune response to an antigen leading to tissue injury, disease, or death in a sensitized individual.
    • An exaggerated response of the immune system to an antigen.
    • Prior exposure to the allergen (antigen) is required for sensitization.
    • Almost any substance capable of inducing an immune response can be an allergen.
    • Genetic susceptibility plays a role, with certain genes (e.g., HLA genes) increasing the risk of hypersensitivity disorders.
    • The development of hypersensitivity to a specific allergen is due to a complex interaction of genetic susceptibility and exposure.

    Types of Hypersensitivity Reactions

    • Type I (Immediate) Hypersensitivity: Allergic or atopic disorders, rapid reaction (within 5-10 minutes) mediated by IgE antibodies.
    • Type II Hypersensitivity (Antibody-Mediated Disorder): Antibodies directed against specific antigens fixed on cell surfaces cause lysis of target cells, mediated by IgG and IgM antibodies.
    • Type III Hypersensitivity (Immune Complex Mediated Disorders): Antigen-antibody complexes deposit in tissues and activate complement, leading to inflammation.
    • Type IV Hypersensitivity (Cell-Mediated or Delayed Type): Delayed reaction (24-72 hours) mediated by T lymphocytes.

    Type I (Immediate) Hypersensitivity Reactions

    • Occurs in 10-20% of the population.
    • Involves mast cells and basophils as effector cells.
    • Elevated levels of serum IgE are present in atopic individuals
    • Reactions are genetically influenced, often involving individuals with a predisposition to allergies (atopic individuals).
    • Antigens (allergens) include house dust mites, pollens, animal danders, or molds.
    • Examples: Bronchial asthma, hay fever, food allergies.

    Mechanism of Type I Hypersensitivity

    Initial Exposure to Antigen (Sensitization)

    • Exposure to sensitizing antigen via inhalation, ingestion, or injection.
    • Presentation of the antigen to T cells by antigen-presenting cells (APCs) like macrophages.
    • T cells differentiate into TH2 cells.
    • Activation of TH2 cells leads to the secretion of cytokines (IL-4, IL-5, and IL-13).
    • IL-4 stimulates B cells to secrete IgE antibodies.
    • IL-5 activates eosinophils, and IL-13 stimulates epithelial cells to secrete mucus.
    • IgE antibodies attach to Fc receptors on mast cells and basophils.
    • No immediate reaction occurs during the initial exposure; sensitization is the primary step.

    Re-exposure to Antigen (Re-challenge)

    • Re-exposure to the allergen crosslinks the IgE molecules on mast cells or basophils.
    • This crosslinking activates the cells, leading to degranulation.
    • Degranulation releases mediators, including histamine, cytokines, prostaglandins, and leukotrienes.

    Two Phases of IgE Triggered Reactions:

    • Immediate Phase Response: Occurs 5-30 minutes after exposure, subsiding within 60 minutes. Pre-formed mediators like histamine, proteases, and chemotactic factors are released. Characterized by vasodilation, vascular leakage, smooth muscle spasm, and glandular secretions.
    • Late-Phase Reaction: Starts 2-8 hours after antigen exposure, lasting several days; involves the release of secondary mediators (prostaglandins, leukotrienes, cytokines, and platelet-activating factor (PAF)) from mast cells. Characterized by tissue infiltration with eosinophils, neutrophils, basophils, monocytes, and TH2 cells, and mucosal epithelial cell damage.

    Localized Type I Hypersensitivity

    • Examples: Hay fever and extrinsic asthma - both tend to run in families and are often preceded by atopic eczema in infancy or childhood.
    • Hay fever: Acute inflammation of the nasal and conjunctival mucosae with sneezing and hypersecretion following exposure to allergens (e.g., grass pollen, food).
    • Bronchial Asthma: Wheezing and acute respiratory distress due to bronchospasm and increased mucus secretion after exposure to house dust or animal dander.

    Systemic Type I Hypersensitivity

    • Anaphylactic reaction: Hypotension, widespread urticaria, and dyspnea.
    • May be life-threatening (anaphylactic shock) and can occur following injection of drugs (e.g., penicillin) in sensitive individuals.

    2. Antibody-Mediated (Type II) Hypersensitivity Reactions

    • Antibodies directed against specific antigens fixed on cell surfaces cause lysis of target cells.
    • Primarily mediated by IgG antibodies (rarely IgM).
    • Antigens can be endogenous or exogenous:
      • Endogenous antigens: Self-antigens.
      • Exogenous antigens: May be adsorbed on a cell surface or extracellular matrix, or may cause altered surface antigens (e.g., drug metabolite).

    Mechanisms of Injury in Type II Hypersensitivity

    • Complement-Dependent Hypersensitivity: C3b (complement) and IgG/IgM antibodies lead to opsonization and phagocytosis or direct cell lysis.
    • Antibody-Dependent Cellular Cytotoxicity (ADCC): Antibody connects natural killer cells or macrophages to the target cell, triggering the release of perforin and granzyme (without phagocytosis or complement activation).
    • Antibody-Mediated Cellular Dysfunction: Antibodies directed against cell surface receptors impair or dysregulate function without causing cell injury or inflammation.

    Examples of Type II Hypersensitivity

    • Antibodies to Blood Cells:
      • Autoimmune hemolytic anemia
      • Transfusion reactions
      • Hemolytic disease of the newborn (erythroblastosis fetalis)
      • Idiopathic thrombocytopenic purpura (ITP)
      • Drug-induced cytotoxic antibodies
    • Antibodies to Tissue Components:
      • Hashimoto thyroiditis: Antibodies against TSH receptors (hypothyroidism).
      • Grave's disease: Antibodies against TSH receptors act as TSH, causing hyperthyroidism.

    Hypersensitivity Reactions

    • Hypersensitivity reactions are exaggerated immune responses to antigens, causing tissue damage, disease, and sometimes death.
    • The immune system is primed or sensitized through prior exposure to the allergen, making it sensitive to future exposures.
    • Almost any substance can act as an allergen (antigen) and trigger a reaction.
    • Genetic predisposition plays a crucial role in the development of hypersensitivity diseases.
    • The interaction between genetic susceptibility and environmental exposure contributes to the development of hypersensitivity.
    • Antigens can be either exogenous (from external sources) or endogenous (from within the body).
    • Exogenous antigens include materials like dust, pollens, foods, drugs, microbes, chemicals, and blood products.
    • Endogenous antigens are self-antigens, typically triggering autoimmune reactions.

    Classification of Hypersensitivity Reactions

    • Type I (Immediate) Hypersensitivity: Known as allergic or atopic disorders, caused by allergens.
    • Type II Hypersensitivity (Antibody-mediated Disorder): Antibodies directed against specific antigens on cell surfaces cause cell lysis.
    • Type III Hypersensitivity (Immune Complex-mediated Disorders): Immune complexes (antigen-antibody complexes) deposit in tissues, causing inflammation and tissue damage.
    • Type IV Hypersensitivity (Cell-mediated or Delayed-type): T cell-mediated response leading to delayed inflammation and tissue damage.

    Type I (Immediate) Hypersensitivity Reactions

    • 10-20% of the population experiences Type I hypersensitivity.
    • Reactions occur rapidly within minutes after allergen exposure.
    • Mediated by IgE antibodies, which bind to mast cells.
    • Individuals with atopic allergies have elevated levels of serum IgE.
    • Reactions occur in genetically predisposed individuals previously sensitized to allergens.
    • Common allergens include house dust mites, pollens, animal danders, and molds.
    • Typical examples include bronchial asthma, hay fever, and food allergies.

    Mechanism of Type I Hypersensitivity

    • A. Initial Exposure to Antigen (Sensitization)*

    • First exposure occurs through inhalation, ingestion, or injection.

    • The allergen is presented to T cells by antigen-presenting cells (APCs) such as macrophages.

    • T cells differentiate into TH2 cells.

    • TH2 cells secrete cytokines (IL-4, IL-5, IL-13) in genetically predisposed individuals.

    • IL-4 stimulates B cells to produce IgE antibodies, which bind to Fc receptors on mast cells and basophils, sensitizing them.

    • IL-5 activates eosinophils, and IL-13 stimulates epithelial cells to secrete mucus.

    • B. Re-exposure to Antigen*

    • Upon re-exposure, the allergen crosslinks IgE molecules on mast cell or basophil surfaces, activating them.

    • Mast cells and basophils degranulate, releasing various mediators like histamine, cytokines, prostaglandins, and leukotrienes.

    Phases of IgE-Triggered Reactions

    • 1. Immediate Phase Response (5 - 30 minutes)*

    • Immediate release of preformed mediators (histamine, proteases, and chemotactic factors).

    • Causes vasodilation, vascular leakage, smooth muscle spasm, and glandular secretions.

    • 2. Late-phase Reaction (2 - 8 hours)*

    • Release of secondary mediators (prostaglandins, leukotrienes, cytokines, and platelet-activating factor) from mast cells.

    • Characterized by infiltration of tissues with eosinophils, neutrophils, basophils, monocytes, and TH2 cells.

    • Results in mucosal epithelial cell damage.

    Examples of Localized Type I Hypersensitivity

    • Hay fever and extrinsic asthma commonly afflict families and often precede atopic eczema in early childhood.
    • Allergic rhinitis causes inflammation of nasal and conjunctival mucosae, with sneezing and hypersecretion following exposure to allergens like grass pollen or food.
    • Bronchial asthma causes wheezing and acute respiratory distress due to bronchospasm and increased mucus secretion after exposure to dust or animal dander.

    Examples of Systemic Type I Hypersensitivity

    • Anaphylaxis, characterized by hypotension, widespread urticaria, and dyspnea.
    • Anaphylactic shock often occurs following injection of drugs like penicillin in sensitive individuals.
    • Anaphylaxis is a medical emergency that can be fatal.

    Inflammation in Localized Type I Hypersensitivity

    • Nasal masses demonstrate edematous stroma with inflammatory cell infiltrates (mainly eosinophils), covered by ciliated columnar epithelium.
    • An allergic nasal polyp is a characteristic sign of this inflammatory process.

    Antibody-mediated (Type II) Hypersensitivity Reactions

    • Antibodies target specific antigens on cell surfaces, disrupting the cell's function and leading to cell lysis.
    • Typically mediated by IgG antibodies, and less commonly IgM antibodies.

    Antigens involved in Type II Hypersensitivity

    • Endogenous antigens: Self-antigens.
    • Exogenous antigens: Adsorbed onto cell surfaces or extracellular matrix, causing altered surface antigens.

    Mechanisms of Injury in Type II Hypersensitivity

    • Complement-dependent HSR
      • Complement activation and lysis of target cells through opsonization and phagocytosis.
      • Involves C3b of the complement system and IgG or IgM antibodies.
    • Antibody-dependent Cellular Cytotoxicity (ADCC)
      • Antibodies link natural killer cells or macrophages to the antigen on the target cell surface.
      • Perforin and granzyme released by these cells disrupt the target cell membrane.
    • Antibody-mediated Cellular Dysfunction
      • Antibodies target cell surface receptors, blocking or impairing their function.
      • Leads to dysfunctional cells, without directly causing cell injury or inflammation.

    Examples of Type II Hypersensitivity Reactions

    • Antibodies to Blood Cells
      • Autoimmune hemolytic anemia
      • Transfusion reactions
      • Hemolytic disease of the newborn (erythroblastosis fetalis)
      • Idiopathic thrombocytopenic purpura (ITP)
      • Drug-induced cytotoxic antibodies
    • ** Antibodies to Tissue Components**
      • Hashimoto thyroiditis: Antibodies against TSH receptor of thyroid epithelial cells.
      • Grave's disease: Antibodies against TSH receptor, acting as TSH and causing hyperthyroidism.

    Hypersensitivity Reactions

    • Definition: An exaggerated and harmful immune response to an antigen, leading to tissue damage, illness, or even death in a previously sensitized individual.

    General Features of Hypersensitivity Disorders

    • Priming/Sensitization: Prior exposure to the allergen is necessary for the immune system to become sensitized.
    • Allergen Potential: Almost any substance that can trigger an immune response can act as an allergen.
    • Genetic Susceptibility: Individuals inherit genes, like HLA genes, that increase their risk of developing hypersensitivity diseases.
    • Complex Interactions: A combination of genetic predisposition and environmental exposure is essential for hypersensitivity development.
    • Antigen Sources: Allergens can originate from external sources (exogenous) or internally (endogenous).
      • Exogenous antigens: Substances like dust, pollen, foods, drugs, microbes, chemicals, and certain blood products.
      • Endogenous antigens: The body's own antigens (self-antigens).

    Classification of Hypersensitivity Reactions

    • Type I (Immediate) Hypersensitivity
    • Type II Hypersensitivity (Antibody-Mediated)
    • Type III Hypersensitivity (Immune Complex-Mediated)
    • Type IV Hypersensitivity (Cell-Mediated/Delayed Type)

    Type I (Immediate) Hypersensitivity Reactions

    • Also known as allergic or atopic disorders.
    • Definition: A rapid (within 5-10 minutes) reaction triggered by antigen (allergen) interacting with IgE antibodies bound to mast cells in a sensitized individual.
    • Prevalence: Affects approximately 10-20% of the population.
    • Mechanism:
      • Initial Exposure (Sensitization):
        1. Allergen Exposure: Inhalation, ingestion, or injection of the allergen.
        2. Antigen Presentation: The allergen is presented to T cells by antigen-presenting cells (APCs), such as macrophages.
        3. TH2 Cell Activation: In genetically susceptible individuals, the allergen activates TH2 cells (a type of CD4+ helper T cell), which release cytokines like IL-4, IL-5, and IL-13.
        4. IgE Antibody Production: IL-4 stimulates B cells to produce cytotropic IgE antibodies.
        5. Mast Cell Sensitization:
        • Mast cells are concentrated near blood vessels, nerves, and in subepithelial tissues.
        • They have Fc receptors that bind IgE antibodies with high affinity.
        • IgE antibodies attach to the Fc receptors on mast cells and basophils.
      • Re-exposure to the Allergen:
        • The allergen cross-links IgE molecules on the surface of mast cells or basophils.
        • This triggers cell activation and degranulation, releasing mediators like histamine, cytokines, prostaglandins, and leukotrienes.
        • Mediators cause immediate symptoms such as vasodilation, increased vascular permeability, increased glandular secretion, and smooth muscle contraction.

    IgE Triggered Reactions

    • Immediate Phase Response (5-30 minutes):
      • Release of preformed mediators like histamine, proteases, and chemotactic factors.
      • Symptoms include vasodilation, leakage of fluids from vessels, smooth muscle spasms, and glandular secretions.
    • Late-Phase Reaction (2-8 hours):
      • Release of secondary mediators from mast cells, including prostaglandins, leukotrienes, cytokines, and platelet-activating factor (PAF).
      • Tissues become infiltrated by eosinophils, neutrophils, basophils, monocytes, and TH2 cells.
      • Mucosal epithelial cell damage occurs.

    Examples of Type I Hypersensitivity

    • Localized Type I Hypersensitivity:
      • Hay Fever (Allergic Rhinitis): Inflammation of the nasal and conjunctival (eye) mucous membranes, causing sneezing, hypersecretion, and other symptoms after exposure to allergens like grass pollen.
      • Extrinsic Asthma: Wheezing, coughing, and respiratory distress due to bronchospasm and increased mucus secretion in the airways, often triggered by allergens like house dust mites or animal dander.
    • Systemic Type I Hypersensitivity (Anaphylaxis):
      • Anaphylactic Shock: Life-threatening condition characterized by hypotension (low blood pressure), widespread hives, and difficulty breathing.
      • Causes: Drug reactions (e.g., penicillin), insect stings, food allergies.

    Inflammation due to Type I Hypersensitivity

    • Nasal Polyps: Edematous tissue with inflammatory cells (mainly eosinophils) covered by ciliated columnar epithelium.

    2. Antibody-Mediated (Type II) Hypersensitivity Reactions

    • Definition: Antibodies directed against specific antigens on cell surfaces cause the destruction of target cells.
    • Characteristics:
      • Antibodies Involved: Primarily IgG, with occasional IgM involvement.
      • Antigens:
        • Endogenous Antigens: Self-antigens.
        • Exogenous Antigens: Foreign substances that get adsorbed onto cell surfaces or extracellular matrix, or lead to altered surface antigens (e.g., drug metabolites).
    • Mechanisms of Injury:
      1. Complement-Dependent Hypersensitivity Reactions (CDCH):
      • Mechanism: Antibodies bind to cell surface antigens, activating the complement system.
      • Effects: Opsonization (marking cells for phagocytosis) and cell lysis.
      • Examples: Transfusion reactions (incompatibility due to ABO or Rh blood groups).
      1. Antibody-Dependent Cellular Cytotoxicity (ADCC):
      • Mechanism: Antibodies attach to target cells, bringing in natural killer (NK) cells or macrophages to destroy the cells without phagocytosis or complement activation.
      • Example: Antibody-dependent destruction of cells infected with viruses.
      1. Antibody-Mediated Cellular Dysfunction:
      • Mechanism: Antibodies target cell surface receptors, leading to impaired or dysfunctional receptor function without direct cell injury or inflammation.
      • Examples:
        • Hashimoto's Thyroiditis: Autoantibodies block the TSH receptor on thyroid cells, leading to hypothyroidism.
        • Grave's Disease (Hyperthyroidism): Autoantibodies stimulate the TSH receptor, causing overproduction of thyroid hormones.

    Examples of Type II Hypersensitivity

    • Blood Cells:
      • Autoimmune Haemolytic Anaemia (AIHA): Antibodies destroy red blood cells.
      • Transfusion Reactions: Incompatible blood transfusions.
      • Haemolytic Disease of the Newborn (Erythroblastosis Foetalis): Maternal antibodies attack fetal red blood cells, causing anemia.
      • Idiopathic Thrombocytopenic Purpura (ITP): Antibodies destroy platelets, causing bleeding problems.
      • Drug-induced Cytotoxic Antibodies: Drugs can trigger immune responses that target cells.
    • Tissue Components:
      • Goodpasture's Syndrome: Antibodies target lung and kidney basement membranes, leading to lung and kidney damage.
      • Myasthenia Gravis: Antibodies block acetylcholine receptors at neuromuscular junctions, causing muscle weakness.

    Hypersensitivity Reactions

    • Definition: An exaggerated immune response to an antigen, leading to tissue damage, disease, or death.
    • Characteristics:
      • Priming: Prior exposure to the allergen is required.
      • Genetic Susceptibility: Inherited genes influence susceptibility.
      • Almost any substance can be an allergen: Allergens can be exogenous or endogenous.

    Types of Hypersensitivity Reactions

    • Type I (Immediate): Also known as allergic or atopic reactions. It occurs within minutes of exposure to an allergen.
      • Mediated by IgE antibodies: Atopic individuals have elevated levels of IgE.
      • Involves mast cell degranulation: Triggers the release of mediators like histamine, leukotrienes, and prostaglandins, causing rapid symptoms.
      • Examples: Bronchial asthma, hay fever, food allergies.

    Type I Hypersensitivity Mechanism

    • Initial Exposure (Sensitization):

      • Exposure: Inhalation, ingestion, or injection of allergen.
      • Antigen Presentation: Allergen is presented by antigen-presenting cells (APCs) to T cells.
      • TH2 Cell Activation: T cells differentiate into TH2 cells, producing cytokines like IL-4, IL-5, and IL-13.
      • IgE Production: IL-4 stimulates B cells to produce IgE antibodies.
      • Mast Cell Sensitization: IgE antibodies bind to Fc receptors on mast cells, preparing them for future allergen exposure.

    • Re-exposure to Antigen:

      • Allergen Cross-linking: Allergen binds to IgE on mast cells, triggering degranulation.
      • Mediator Release: Pre-formed mediators (histamine, proteases, etc.) cause immediate effects.
      • Late-Phase Reaction: Secondary mediators (prostaglandins, leukotrienes, cytokines) cause inflammation and tissue damage.

    Type II Hypersensitivity (Antibody-Mediated)

    • Definition: Antibodies targeting cell-surface antigens cause cell lysis or dysfunction.
    • Characteristics:
      • Antibodies: Primarily IgG, sometimes IgM.
      • Antigens: Can be endogenous (self) or exogenous (absorbed or modified cell surface antigens).
    • Mechanisms of Injury:
      • Complement-Dependent: Complement activation leading to cell lysis (e.g., transfusion reactions).
      • Antibody-Dependent Cellular Cytotoxicity (ADCC): Antibodies trigger natural killer cells or macrophages to destroy target cells without phagocytosis.
      • Antibody-Mediated Cellular Dysfunction: Antibodies impair receptor function without causing cell death (e.g., Grave's disease, Hashimoto's thyroiditis).

    Examples of Type II Hypersensitivity

    • Blood Cells:
      • Autoimmune hemolytic anemia, transfusion reactions, hemolytic disease of the newborn, idiopathic thrombocytopenic purpura.
    • Tissue Components:
      • Myasthenia gravis, Goodpasture's syndrome, pemphigus vulgaris, rheumatoid arthritis.

    Type III Hypersensitivity (Immune Complex-Mediated)

    • Definition: Formation of antigen-antibody complexes, depositing in tissues and triggering inflammation.
    • Characteristics:
      • Antibodies: Primarily IgG
      • Antigens: Soluble antigens, like bacterial products or self-antigens.
      • Complex Deposition: Complexes form in circulation and deposit in tissues.
    • Mechanism:
      • Complement Activation: Immune complexes activate complement, attracting inflammatory cells.
      • Neutrophil Recruitment: Neutrophils are attracted to the site, releasing enzymes and causing tissue damage.
      • Examples: Serum sickness, systemic lupus erythematosus.

    Type IV Hypersensitivity (Cell-Mediated/Delayed Type)

    • Definition: T cell-mediated immune response against antigens, resulting in delayed inflammation.
    • Characteristics:
      • Delayed Reaction: Symptoms develop 24-72 hours after exposure.
      • T Cells: Primarily CD4+ T cells (TH1 or TH17).
      • Mediators: Cytokines, such as TNF-α, IFN-γ, and IL-17.
    • Mechanisms:
      • Antigen Presentation: Antigen is presented by APCs to T cells.
      • T Cell Activation: TH1 or TH17 cells are activated and release cytokines.
      • Inflammation: Cytokines attract macrophages and cause tissue damage.
    • Examples: Contact dermatitis, tuberculin reaction, graft rejection, some autoimmune diseases.

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    Description

    This quiz delves into hypersensitivity reactions, explaining their pathological nature and the immune responses involved. You will explore different types of hypersensitivity, including Type I and Type II, and understand the role of genetic factors and allergens in these processes.

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