Podcast
Questions and Answers
What is the primary characteristic of Type I hypersensitivity reactions?
What is the primary characteristic of Type I hypersensitivity reactions?
- It occurs several hours after exposure to an allergen.
- It causes immune complex formation.
- It involves mast cells and IgE antibodies. (correct)
- It is mediated by IgG antibodies.
Which of the following best describes an exogenous antigen?
Which of the following best describes an exogenous antigen?
- Antigens produced by the body due to autoimmune reactions.
- Antigens derived from environmental sources such as dust or pollen. (correct)
- Antigens that are primarily genetic in origin.
- Protein fragments created as a immune response in the host.
What role do HLA genes play in hypersensitivity disorders?
What role do HLA genes play in hypersensitivity disorders?
- They are responsible for storing histamine in mast cells.
- They enhance the immune response to all allergens equally.
- They contribute to genetic susceptibility to hypersensitivity diseases. (correct)
- They help in the elimination of self-antigens.
Which of the following statements is TRUE regarding Type II hypersensitivity reactions?
Which of the following statements is TRUE regarding Type II hypersensitivity reactions?
In which percentage of the population do Type I hypersensitivity reactions typically occur?
In which percentage of the population do Type I hypersensitivity reactions typically occur?
What triggers the immediate reaction seen in Type I hypersensitivity?
What triggers the immediate reaction seen in Type I hypersensitivity?
Which type of hypersensitivity involves immune complex-mediated disorders?
Which type of hypersensitivity involves immune complex-mediated disorders?
Which of the following is NOT a feature of hypersensitivity disorders?
Which of the following is NOT a feature of hypersensitivity disorders?
What is necessary for an individual to be classified as genetically susceptible to type I hypersensitivity reactions?
What is necessary for an individual to be classified as genetically susceptible to type I hypersensitivity reactions?
Which cytokine primarily stimulates B cells to produce IgE antibodies during the sensitization process?
Which cytokine primarily stimulates B cells to produce IgE antibodies during the sensitization process?
What is the primary role of mast cells in type I hypersensitivity reactions?
What is the primary role of mast cells in type I hypersensitivity reactions?
What triggers the degranulation of mast cells during re-exposure to an allergen?
What triggers the degranulation of mast cells during re-exposure to an allergen?
During which phase of an allergic reaction do symptoms typically begin to manifest after allergen exposure?
During which phase of an allergic reaction do symptoms typically begin to manifest after allergen exposure?
What is a characteristic feature of the immediate phase response in type I hypersensitivity?
What is a characteristic feature of the immediate phase response in type I hypersensitivity?
In the context of allergic reactions, what is the function of eosinophils activated by IL-5?
In the context of allergic reactions, what is the function of eosinophils activated by IL-5?
What type of cells are primarily linked to the initiation of type I hypersensitivity reactions through antigen presentation?
What type of cells are primarily linked to the initiation of type I hypersensitivity reactions through antigen presentation?
What is a characteristic feature of the early-phase reaction in type I hypersensitivity?
What is a characteristic feature of the early-phase reaction in type I hypersensitivity?
Which of the following best describes the late-phase reaction in type I hypersensitivity?
Which of the following best describes the late-phase reaction in type I hypersensitivity?
What type of hypersensitivity includes conditions such as hay fever and extrinsic asthma?
What type of hypersensitivity includes conditions such as hay fever and extrinsic asthma?
What might a systemic type I hypersensitivity reaction lead to if severe?
What might a systemic type I hypersensitivity reaction lead to if severe?
In type II hypersensitivity reactions, which antibodies are most commonly involved?
In type II hypersensitivity reactions, which antibodies are most commonly involved?
Which mechanism is NOT a potential effect of the antigen-antibody reaction in type II hypersensitivity?
Which mechanism is NOT a potential effect of the antigen-antibody reaction in type II hypersensitivity?
What type of inflammatory infiltrate is primarily observed in allergic nasal polyps associated with type I hypersensitivity?
What type of inflammatory infiltrate is primarily observed in allergic nasal polyps associated with type I hypersensitivity?
Which of the following correctly describes the role of secondary mediators in the late-phase reaction of type I hypersensitivity?
Which of the following correctly describes the role of secondary mediators in the late-phase reaction of type I hypersensitivity?
What is the primary mechanism by which antibodies lead to the lysis of target cells in Type II hypersensitivity reactions?
What is the primary mechanism by which antibodies lead to the lysis of target cells in Type II hypersensitivity reactions?
In the context of antibody-dependent cellular cytotoxicity (ADCC), which component directly links natural killer cells to target cells?
In the context of antibody-dependent cellular cytotoxicity (ADCC), which component directly links natural killer cells to target cells?
Which of the following conditions is associated with antibodies that act as agonists on their target receptors?
Which of the following conditions is associated with antibodies that act as agonists on their target receptors?
What type of blood cells are primarily involved in hemolytic disease of the newborn (erythroblastosis foetalis)?
What type of blood cells are primarily involved in hemolytic disease of the newborn (erythroblastosis foetalis)?
Which type of immune response is characterized by the opsonization of cells and their subsequent phagocytosis by macrophages?
Which type of immune response is characterized by the opsonization of cells and their subsequent phagocytosis by macrophages?
Which of the following is NOT a characteristic of Type II hypersensitivity reactions?
Which of the following is NOT a characteristic of Type II hypersensitivity reactions?
What is the consequence of penicillin binding to red blood cells in the context of Type II hypersensitivity?
What is the consequence of penicillin binding to red blood cells in the context of Type II hypersensitivity?
What type of antibodies cause ineffective cell function without direct injury or inflammation in conditions such as Hashimoto's thyroiditis?
What type of antibodies cause ineffective cell function without direct injury or inflammation in conditions such as Hashimoto's thyroiditis?
Study Notes
Hypersensitivity Reactions
- Hypersensitivity reaction is an exaggerated immune response to an antigen leading to tissue damage, disease, or even death in a previously sensitized individual
- Hypersensitivity reactions are classified into four main types: Type I, Type II, Type III, and Type IV
Type I (Immediate) Hypersensitivity Reactions
- Also known as allergic or atopic reactions
- Occurs within minutes (5-10 minutes) after antigen (allergen) interacts with IgE antibodies bound to mast cells
- Mediated by IgE antibodies
- Develops in genetically susceptible individuals who are atopic
- Common examples include bronchial asthma, hay fever, and food allergies
Mechanism of Type I Hypersensitivity Reactions
-
Initial Exposure (Sensitization)
- Antigen (allergen) enters the body through inhalation, ingestion, or injection
- Antigen is presented to T cells by antigen-presenting cells (APCs) like macrophages
- T cells differentiate into TH2 cells
- TH2 cells release cytokines (IL-4, IL-5, and IL-13)
- IL-4 stimulates B cells to produce IgE antibodies
- IL-5 activates eosinophils
- IL-13 stimulates epithelial cells to produce mucus
- IgE antibodies bind to Fc receptors on mast cells and basophils
-
Re-exposure to Antigen (Degranulation)
- Re-exposure cross-links IgE molecules on mast cells and basophils
- This triggers degranulation, releasing mediators like histamine, cytokines, prostaglandins, and leukotrienes
- Mediators cause immediate reactions: vasodilation, increased vascular permeability, smooth muscle contraction, increased glandular secretions
- Late-phase reaction (2-8 hours) involves release of secondary mediators, tissue infiltration by inflammatory cells, and mucosal damage
Localized Type I Hypersensitivity Reactions
- Examples: Hay fever and extrinsic asthma
- Hay fever: Acute inflammation of the nasal and conjunctival mucosa with sneezing and hypersecretion after allergen exposure
- Bronchial asthma: Wheezing and respiratory distress caused by bronchospasm and increased mucus secretion after allergen exposure
Systemic Type I Hypersensitivity Reactions
- Anaphylactic reactions: Severe, life-threatening allergic response characterized by shock, hypotension, widespread urticaria, and dyspnea
- Often triggered by drug injections, food allergies, or insect stings
Type II (Antibody-Mediated) Hypersensitivity Reactions
- Antibodies directed against specific antigens on cell surfaces cause cell lysis or dysfunction
- Mediated by IgG (usually) and IgM (rarely) antibodies
- Antigens can be endogenous (self) or exogenous (adsorbed on cell surfaces or extracellular matrix)
- Mechanisms:
- Complement-dependent cytotoxicity
- Antibody-dependent cellular cytotoxicity (ADCC)
- Antibody-mediated cellular dysfunction (e.g. Graves' disease, Hashimoto's thyroiditis)
Complement-Dependent Cytotoxicity (Type II Hypersensitivity)
- Antibodies activate complement system, leading to cell lysis
- Examples:
- Transfusion reactions (ABO or Rh incompatibility)
- Autoimmune hemolytic anemia
Antibody-Dependent Cellular Cytotoxicity (ADCC) (Type II Hypersensitivity)
- Antibodies bind to target cells, facilitating their destruction by NK cells or macrophages
- Does not involve complement activation or phagocytosis
- Target cell killing occurs through the release of perforin and granzyme by NK cells
Antibody-Mediated Cellular Dysfunction (Type II Hypersensitivity)
- Antibodies block or interfere with cell surface receptor function
- Examples:
- Hashimoto's thyroiditis: Antibodies against TSH receptor block TSH binding, leading to hypothyroidism
- Graves' disease: Antibodies against TSH receptor act as TSH, leading to hyperthyroidism
Examples of Type II Hypersensitivity Reactions
-
Blood cells:
- Autoimmune hemolytic anemia
- Transfusion reactions
- Hemolytic disease of the newborn (erythroblastosis fetalis)
- Idiopathic thrombocytopenic purpura (ITP)
- Drug-induced cytotoxic antibodies
-
Tissue components:
- Myasthenia gravis (antibodies against acetylcholine receptor)
- Goodpasture's syndrome (antibodies against basement membrane of kidneys and lungs)
- Pemphigus vulgaris (antibodies against desmosomes in skin)
###Â Note: This is not an exhaustive list of all the details included in the document but a summarized structure of key topics and their essential details.
Studying That Suits You
Use AI to generate personalized quizzes and flashcards to suit your learning preferences.
Related Documents
Description
Test your knowledge on hypersensitivity reactions, focusing on the types and mechanisms involved. This quiz covers Type I (Immediate) hypersensitivity reactions, their triggers, and the biological responses elicited. Perfect for students of immunology or medical sciences.
