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What is an example of a Type IV hypersensitivity reaction?
What is an example of a Type IV hypersensitivity reaction?
What type of cells are involved in the cytolytic T cell response to poison ivy?
What type of cells are involved in the cytolytic T cell response to poison ivy?
CD8 T cells
Which of the following diseases can involve Type IV hypersensitivity?
Which of the following diseases can involve Type IV hypersensitivity?
All diseases only involve one type of hypersensitivity reaction.
All diseases only involve one type of hypersensitivity reaction.
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What is characterized by mononuclear cell infiltration of the dermis?
What is characterized by mononuclear cell infiltration of the dermis?
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What is meant by the term 'immunopathology'?
What is meant by the term 'immunopathology'?
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Which of the following describes hypersensitivity?
Which of the following describes hypersensitivity?
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How many types of hypersensitivity reactions are there?
How many types of hypersensitivity reactions are there?
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What type of hypersensitivity reaction is mediated by IgE?
What type of hypersensitivity reaction is mediated by IgE?
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Name one hallmark of the late-phase reaction in Type I hypersensitivity.
Name one hallmark of the late-phase reaction in Type I hypersensitivity.
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In Type II hypersensitivity, antibodies are produced against ______ antigens.
In Type II hypersensitivity, antibodies are produced against ______ antigens.
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What is a classic example of a Type III hypersensitivity disease?
What is a classic example of a Type III hypersensitivity disease?
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Which type of hypersensitivity reaction is mediated primarily by T cells?
Which type of hypersensitivity reaction is mediated primarily by T cells?
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What type of cells are the effector cells in Type IV hypersensitivity reactions?
What type of cells are the effector cells in Type IV hypersensitivity reactions?
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What is a granuloma reaction?
What is a granuloma reaction?
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What role do mast cells play in Type I hypersensitivity?
What role do mast cells play in Type I hypersensitivity?
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Anaphylaxis is an example of a ______ reaction.
Anaphylaxis is an example of a ______ reaction.
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Which type of antibody is primarily involved in mediating Type I hypersensitivity reactions?
Which type of antibody is primarily involved in mediating Type I hypersensitivity reactions?
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What distinguishes Type II hypersensitivity from Type III hypersensitivity reactions?
What distinguishes Type II hypersensitivity from Type III hypersensitivity reactions?
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Which disease is commonly associated with Type III hypersensitivity reactions?
Which disease is commonly associated with Type III hypersensitivity reactions?
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In the context of immunopathology, which statement about mast cells in Type I hypersensitivity is accurate?
In the context of immunopathology, which statement about mast cells in Type I hypersensitivity is accurate?
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What is a key component in the pathogenesis of autoimmune diseases related to hypersensitivity reactions?
What is a key component in the pathogenesis of autoimmune diseases related to hypersensitivity reactions?
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What is a critical effect of chronic exposure to allergens on the airways?
What is a critical effect of chronic exposure to allergens on the airways?
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Which statement accurately describes the mechanism of Type II hypersensitivity?
Which statement accurately describes the mechanism of Type II hypersensitivity?
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What is the primary function of vasoactive amines released from mast cell granules during an acute inflammatory response?
What is the primary function of vasoactive amines released from mast cell granules during an acute inflammatory response?
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What triggers the systemic reaction of anaphylaxis?
What triggers the systemic reaction of anaphylaxis?
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Which of the following mediators is associated with the late-phase reaction in Type I hypersensitivity?
Which of the following mediators is associated with the late-phase reaction in Type I hypersensitivity?
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What characterizes the sensitization phase in Type II hypersensitivity?
What characterizes the sensitization phase in Type II hypersensitivity?
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What genetic predisposition increases the likelihood of IgE production in certain individuals?
What genetic predisposition increases the likelihood of IgE production in certain individuals?
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Which of the following diseases exemplifies Type II hypersensitivity?
Which of the following diseases exemplifies Type II hypersensitivity?
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Which of the following conditions is NOT typically associated with Type I hypersensitivity reactions?
Which of the following conditions is NOT typically associated with Type I hypersensitivity reactions?
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What characterizes the initial response during the acute inflammatory reaction mediated by mast cell degranulation?
What characterizes the initial response during the acute inflammatory reaction mediated by mast cell degranulation?
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What is the potential outcome of the systemic reaction of anaphylaxis if not treated promptly?
What is the potential outcome of the systemic reaction of anaphylaxis if not treated promptly?
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Which statement best describes why certain antigens preferentially induce an IgE response?
Which statement best describes why certain antigens preferentially induce an IgE response?
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What role do phagocytes play in Type II hypersensitivity reactions?
What role do phagocytes play in Type II hypersensitivity reactions?
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Which statement best defines anaphylaxis?
Which statement best defines anaphylaxis?
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In the context of asthma as a Type I hypersensitivity reaction, what is the primary physiological change during a flare-up?
In the context of asthma as a Type I hypersensitivity reaction, what is the primary physiological change during a flare-up?
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What role do proteases released from secretory granules of mast cells play during an acute inflammatory response?
What role do proteases released from secretory granules of mast cells play during an acute inflammatory response?
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In autoimmune hemolytic anemia, what immunological process leads to red blood cell destruction?
In autoimmune hemolytic anemia, what immunological process leads to red blood cell destruction?
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How does mucus overproduction affect airflow in chronic airway exposure?
How does mucus overproduction affect airflow in chronic airway exposure?
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Which characteristic identifies the sensitization phase in Type I hypersensitivity?
Which characteristic identifies the sensitization phase in Type I hypersensitivity?
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What is the primary effector mechanism involved in Type IV hypersensitivity reactions?
What is the primary effector mechanism involved in Type IV hypersensitivity reactions?
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How does IgE contribute to immediate hypersensitivity reactions?
How does IgE contribute to immediate hypersensitivity reactions?
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What distinguishes Type II from Type III hypersensitivity reactions?
What distinguishes Type II from Type III hypersensitivity reactions?
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What is a potential consequence of excessive IgE production in sensitized individuals?
What is a potential consequence of excessive IgE production in sensitized individuals?
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Which factor has contributed to the surge in allergy incidence in developed nations?
Which factor has contributed to the surge in allergy incidence in developed nations?
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What primary characteristic differentiates Type I, II, and III hypersensitivity from Type IV hypersensitivity?
What primary characteristic differentiates Type I, II, and III hypersensitivity from Type IV hypersensitivity?
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Which statement best describes the role of mast cells in Type I hypersensitivity?
Which statement best describes the role of mast cells in Type I hypersensitivity?
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What is the main immune mechanism involved in the pathology of autoimmune diseases related to hypersensitivity?
What is the main immune mechanism involved in the pathology of autoimmune diseases related to hypersensitivity?
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In what way do cytokines released by mast cells affect the body during a Type I hypersensitivity reaction?
In what way do cytokines released by mast cells affect the body during a Type I hypersensitivity reaction?
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Study Notes
Hypersensitivity Reactions Overview
- Hypersensitivity reactions are damaging immune responses against foreign or self-antigens.
- Four types of hypersensitivity reactions exist, classified by immunologic mechanisms (Type I-IV).
- Immunopathology refers to tissue injury resulting from immune reactions, which can be excessive or misdirected.
Types of Hypersensitivity
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Type I (IgE-Mediated)
- Also known as immediate hypersensitivity; symptoms arise within minutes.
- Involves B cells producing IgE that binds to mast cells, leading to degranulation upon re-exposure to the antigen.
- Mediators include vasoactive amines (histamine), lipid mediators (arachidonic acid), and cytokines (TNF, IL-4).
- Examples: seasonal allergies, urticaria, asthma, anaphylaxis, characterized by vascular shock and airway obstruction.
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Type II (Antibody-Mediated Cytotoxicity)
- Involves IgM or IgG antibodies against self-antigens, leading to cell lysis or opsonization for phagocytosis.
- Can alter normal cell function (e.g., myasthenia gravis, Grave’s disease).
- Example: autoimmune hemolytic anemia and Goodpasture’s syndrome, where antibody binding results in tissue damage.
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Type III (Immune-Complex)
- Formed when antibodies combine with soluble antigens, leading to deposition in blood vessel walls and inflammatory response.
- Activation of complement recruits neutrophils, which release enzymes causing tissue damage.
- Examples: systemic lupus erythematosus, post-streptococcal glomerulonephritis, with kidney damage resulting from immune complex deposition.
-
Type IV (T Cell-Mediated)
- Delayed-type hypersensitivity mediated by T cells, exhibiting a slower response (1-3 days).
- Cytokines from TH1 cells recruit macrophages, leading to tissue damage.
- Granuloma formation occurs when antigens persist, limiting spread through walled-off immune responses.
- Examples: contact dermatitis, granulomatous inflammation from tuberculosis, transplant rejection, and some autoimmune disorders like Type 1 Diabetes and Multiple Sclerosis.
Key Mechanisms and Terms
- Sensitization Phase: Initial exposure to an antigen is crucial, as it primes the immune system for subsequent reactions.
- Bi-Phasic Reaction (Type I): Initial acute response followed by a more sustained late-phase response characterized by eosinophil influx.
- Granuloma Reaction: Results from prolonged immune activation, often due to chronic infections or allergens.
- Atopic Individuals: Predisposed to produce IgE due to genetic factors, increasing sensitivity to allergens.
Clinical Context
- Hypersensitivity reactions can lead to various diseases encountered across multiple clinical contexts.
- Increased allergy incidence in developed nations, particularly among children.
- Understanding these mechanisms is vital for diagnosing and managing allergic diseases and autoimmune conditions.
Acute Inflammatory Response
- Characteristic symptoms arise from mast cell mediators initiating an acute inflammatory response.
- Initial response (1-2 hours) involves:
- Vasodilating vasoactive amines (notably histamine) released from mast cell granules.
- Lipid mediators derived from arachidonic acid that promote vascular changes and recruit leukocytes.
- Proteases in granules that degrade extracellular matrix and activate complement.
- Late-phase reaction is typically more pronounced and prolonged, marked by cytokines (e.g., TNF and IL-4) orchestrating the immune response, with eosinophil influx being a distinctive feature.
IgE Production and Allergy
- Only a subset of antigens trigger an IgE response; lower antigen doses favor production.
- Genetics influence IgE production; individuals predisposed to increased T Helper-2 cytokines (like IL-4 and IL-13) are termed atopic.
Hypersensitivity Reactions Overview
- Hypersensitivity refers to exaggerated immune responses to otherwise harmless substances.
- Allergy incidents have surged in developed nations, notably among children.
- Four types of hypersensitivity reactions classified by immunological mechanisms:
- Types I-III involve direct antibody action.
- Type IV is mediated by T cells.
Type I Hypersensitivity (IgE-Mediated)
- Symptoms manifest rapidly (within minutes of antigen exposure).
- Sensitization phase begins with initial antigen exposure leading B cells to produce IgE.
- Secreted IgE binds to high-affinity IgE receptors on mast cells, persisting even in the absence of antigen.
- Upon subsequent antigen exposure, cross-linking of IgE on mast cells results in granule exocytosis and cytokine release, the effector phase.
- Chronic exposure may result in airway remodeling: smooth muscle hypertrophy, thickened basement membrane, and increased mucus production.
Systemic Reactions and Anaphylaxis
- Anaphylaxis entails severe systemic reactions: vascular shock, widespread edema, and respiratory distress due to bronchiole constriction.
- Life-threatening reactions can occur with minimal antigen exposure.
Type II Hypersensitivity (Antibody-Mediated)
- Mechanism involves sensitization whereby antibodies (primarily IgM or IgG) target cellular (self) antigens.
- The antibodies bind to cells or extracellular proteins, leading to complement fixation, cell lysis, or opsonization for phagocytic uptake.
- Examples include autoimmune hemolytic anemia and transfusion reactions.
- Damage can also arise through inflammation without phagocytosis, involving neutrophil activation and local complement activation.
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Description
This quiz covers the fundamental concepts of hypersensitivity reactions as explored in the Foundations block. Instructors Lonnie Lybarger, PhD, and Erika Bracamonte, MD, guide learners through the mechanisms and classifications of these immune responses. Prepare for both theoretical and clinical aspects discussed during the session.