Hypersensitivity

1. Which type of hypersensitivity reaction is mediated by IgE antibodies?
   A. Type I
   B. Type II
   C. Type III
   D. Type IV
   

1. Answer: A. Type I
   Explanation: Type I hypersensitivity is mediated by IgE antibodies, which bind to mast cells and trigger the release of inflammatory mediators like histamine.

1. What is the primary mechanism of tissue damage in Type II hypersensitivity?
   A. Immune complex deposition
   B. Antibody-mediated cell lysis or dysfunction
   C. T cell-mediated cytotoxicity
   D. Mast cell degranulation
   

1. Answer: B. Antibody-mediated cell lysis or dysfunction
   Explanation: Type II hypersensitivity involves antibodies (IgG or IgM) that target cell surface antigens, leading to cell lysis or dysfunction through opsonization, complement activation, or receptor blockade.

1. Which of the following is an example of Type III hypersensitivity?
   A. Anaphylaxis
   B. Autoimmune hemolytic anemia
   C. Systemic lupus erythematosus (SLE)
   D. Contact dermatitis
   .

1. Answer: C. Systemic lupus erythematosus (SLE)
   Explanation: SLE is a Type III hypersensitivity reaction where immune complexes deposit in tissues, causing inflammation and tissue damage

1. What is the primary effector cell in Type IV hypersensitivity?
   A. Mast cells
   B. B cells
   C. T cells
   D. Neutrophils
   

1. Answer: C. T cells
   Explanation: Type IV hypersensitivity is mediated by T cells (CD4+ and CD8+), which either recruit macrophages (DTH) or directly kill target cells (cytotoxic T cell-mediated reactions).

1. Which of the following is a characteristic of Type I hypersensitivity?
   A. Delayed reaction (24-48 hours)
   B. Mediated by IgG antibodies
   C. Rapid reaction (minutes)
   D. Involves immune complex deposition
   

1. Answer: C. Rapid reaction (minutes)
   Explanation: Type I hypersensitivity is characterized by a rapid reaction (within minutes) due to mast cell degranulation triggered by IgE antibodies.

1. What is the role of complement in Type II hypersensitivity?
   A. It activates mast cells
   B. It recruits neutrophils and causes inflammation
   C. It directly kills target cells
   D. It mediates T cell activation
   

1. Answer: B. It recruits neutrophils and causes inflammation
   Explanation: In Type II hypersensitivity, antibodies activate complement, leading to the recruitment of neutrophils and inflammation, which contributes to tissue damage.

1. Which of the following is an example of Type IV hypersensitivity?
   A. Asthma
   B. Myasthenia gravis
   C. Tuberculosis
   D. Post-streptococcal glomerulonephritis
   

1. Answer: C. Tuberculosis
   Explanation: Tuberculosis is an example of Type IV hypersensitivity, where T cells (CD4+) recruit macrophages to form granulomas in response to Mycobacterium tuberculosis.

1. What is the primary mediator released in Type I hypersensitivity?
   A. Interferon-γ
   B. Histamine
   C. Complement
   D. Cytokines
   

1. Answer: B. Histamine
   Explanation: Histamine is one of the primary mediators released by mast cells during Type I hypersensitivity, causing vasodilation, bronchoconstriction, and increased vascular permeability.

1. Which of the following is a systemic Type I hypersensitivity reaction?
   A. Hay fever
   B. Asthma
   C. Anaphylaxis
   D. Atopic dermatitis
   

1. Answer: C. Anaphylaxis
   Explanation: Anaphylaxis is a systemic Type I hypersensitivity reaction characterized by widespread mast cell degranulation, leading to severe vasodilation, hypotension, and shock.

1. What is the primary mechanism of tissue damage in Type III hypersensitivity?
   A. Antibody-mediated cell lysis
   B. Immune complex deposition and complement activation
   C. T cell-mediated cytotoxicity
   D. Mast cell degranulation
   

1. Answer: B. Immune complex deposition and complement activation
   Explanation: Type III hypersensitivity involves the deposition of antigen-antibody complexes in tissues, leading to complement activation, inflammation, and tissue damage.

1. Regarding Type I hypersensitivity:
   A. Type I hypersensitivity is mediated by IgE antibodies.
   B. Type I hypersensitivity reactions occur within minutes of allergen exposure.
   C. Type I hypersensitivity involves T cell-mediated cytotoxicity.
   D. Anaphylaxis is a systemic Type I hypersensitivity reaction.
   E. Type I hypersensitivity is also known as delayed-type hypersensitivity.

1. A. Type I hypersensitivity is mediated by IgE antibodies. (True)
   B. Type I hypersensitivity reactions occur within minutes of allergen exposure. (True)
   C. Type I hypersensitivity involves T cell-mediated cytotoxicity. (False)
   D. Anaphylaxis is a systemic Type I hypersensitivity reaction. (True)
   E. Type I hypersensitivity is also known as delayed-type hypersensitivity. (False)

2. Explanation:

   • Type I hypersensitivity is mediated by IgE antibodies and occurs rapidly (within minutes).

   • Anaphylaxis is a systemic Type I reaction.

   • Type I hypersensitivity does not involve T cells; it is mediated by mast cells and IgE.

   • Delayed-type hypersensitivity refers to Type IV reactions, not Type I.

1. Regarding Type II hypersensitivity:
   A. Type II hypersensitivity is mediated by IgG or IgM antibodies.
   B. Type II hypersensitivity involves immune complex deposition.
   C. Myasthenia gravis is an example of Type II hypersensitivity.
   D. Type II hypersensitivity can lead to complement activation and cell lysis.
   E. Type II hypersensitivity is also known as immune complex-mediated hypersensitivity.

1. A. Type II hypersensitivity is mediated by IgG or IgM antibodies. (True)
   B. Type II hypersensitivity involves immune complex deposition. (False)
   C. Myasthenia gravis is an example of Type II hypersensitivity. (True)
   D. Type II hypersensitivity can lead to complement activation and cell lysis. (True)
   E. Type II hypersensitivity is also known as immune complex-mediated hypersensitivity. (False)

   Explanation:

   • Type II hypersensitivity is mediated by IgG or IgM antibodies, leading to cell lysis or dysfunction.

   • Myasthenia gravis is an example of Type II hypersensitivity, where antibodies block acetylcholine receptors.

   • Immune complex-mediated hypersensitivity refers to Type III, not Type II.

1. Regarding Type III hypersensitivity:
   A. Type III hypersensitivity involves the deposition of antigen-antibody complexes. (True)
   B. Type III hypersensitivity is mediated by T cells.
   C. Systemic lupus erythematosus (SLE) is an example of Type III hypersensitivity.
   D. Type III hypersensitivity can lead to complement activation and inflammation.
   E. Type III hypersensitivity is also known as antibody-mediated cytotoxic hypersensitivity.

1. A. Type III hypersensitivity involves the deposition of antigen-antibody complexes. (True)
   B. Type III hypersensitivity is mediated by T cells. (False)
   C. Systemic lupus erythematosus (SLE) is an example of Type III hypersensitivity. (True)
   D. Type III hypersensitivity can lead to complement activation and inflammation. (True)
   E. Type III hypersensitivity is also known as antibody-mediated cytotoxic hypersensitivity. (False)

   Explanation:

   • Type III hypersensitivity involves immune complex deposition, leading to complement activation and inflammation.

   • SLE is an example of Type III hypersensitivity.

   • Antibody-mediated cytotoxic hypersensitivity refers to Type II, not Type III.

1. Regarding Type IV hypersensitivity:
   A. Type IV hypersensitivity is mediated by T cells.
   B. Type IV hypersensitivity involves IgE antibodies.
   C. Tuberculosis is an example of Type IV hypersensitivity.
   D. Type IV hypersensitivity reactions occur within minutes of antigen exposure.
   E. Type IV hypersensitivity is also known as delayed-type hypersensitivity.

1. A. Type IV hypersensitivity is mediated by T cells. (True)
   B. Type IV hypersensitivity involves IgE antibodies. (False)
   C. Tuberculosis is an example of Type IV hypersensitivity. (True)
   D. Type IV hypersensitivity reactions occur within minutes of antigen exposure. (False)
   E. Type IV hypersensitivity is also known as delayed-type hypersensitivity. (True)

   Explanation:

   • Type IV hypersensitivity is mediated by T cells (CD4+ and CD8+).

   • Tuberculosis is an example of Type IV hypersensitivity, where T cells recruit macrophages to form granulomas.

   • Type IV reactions are delayed, occurring 24-48 hours after antigen exposure.

   • IgE antibodies are involved in Type I, not Type IV hypersensitivity.

1. Regarding hypersensitivity reactions:
   A. Type I hypersensitivity is also known as immediate hypersensitivity.
   B. Type II hypersensitivity involves immune complex deposition.
   C. Type III hypersensitivity can lead to necrotizing vasculitis.
   D. Type IV hypersensitivity is mediated by B cells.
   E. Anaphylaxis is a Type I hypersensitivity reaction.

1. A. Type I hypersensitivity is also known as immediate hypersensitivity. (True)
   B. Type II hypersensitivity involves immune complex deposition. (False)
   C. Type III hypersensitivity can lead to necrotizing vasculitis. (True)
   D. Type IV hypersensitivity is mediated by B cells. (False)
   E. Anaphylaxis is a Type I hypersensitivity reaction. (True)

2. Explanation:

   • Type I hypersensitivity is immediate, mediated by IgE and mast cells.

   • Type II hypersensitivity involves antibody-mediated cell lysis, not immune complex deposition.

   • Type III hypersensitivity can cause necrotizing vasculitis due to immune complex deposition.

   • Type IV hypersensitivity is mediated by T cells, not B cells.

   • Anaphylaxis is a systemic Type I hypersensitivity reaction.

6. Regarding Type I hypersensitivity:
   A. Histamine is the primary mediator released during Type I hypersensitivity.
   B. Type I hypersensitivity reactions can be both systemic and local.
   C. Asthma is an example of a local Type I hypersensitivity reaction.
   D. Type I hypersensitivity is mediated by IgG antibodies.
   E. Anaphylaxis is a systemic Type I hypersensitivity reaction.

6. A. Histamine is the primary mediator released during Type I hypersensitivity. (True)
   B. Type I hypersensitivity reactions can be both systemic and local. (True)
   C. Asthma is an example of a local Type I hypersensitivity reaction. (True)
   D. Type I hypersensitivity is mediated by IgG antibodies. (False)
   E. Anaphylaxis is a systemic Type I hypersensitivity reaction. (True)

   Explanation:

   • Histamine is a key mediator released by mast cells during Type I hypersensitivity.

   • Type I reactions can be systemic (e.g., anaphylaxis) or local (e.g., asthma, hay fever).

   • Asthma is a local Type I reaction affecting the lungs.

   • Type I hypersensitivity is mediated by IgE, not IgG antibodies.

   • Anaphylaxis is a severe systemic Type I reaction.

Regarding Type II hypersensitivity:
A. Type II hypersensitivity can involve opsonization and phagocytosis of target cells.
B. Goodpasture syndrome is an example of Type II hypersensitivity.
C. Type II hypersensitivity is mediated by IgE antibodies.
D. Antibodies in Type II hypersensitivity can cause cellular dysfunction without cell lysis.
E. Transfusion reactions are an example of Type II hypersensitivity.

A. Type II hypersensitivity can involve opsonization and phagocytosis of target cells. (True)
B. Goodpasture syndrome is an example of Type II hypersensitivity. (True)
C. Type II hypersensitivity is mediated by IgE antibodies. (False)
D. Antibodies in Type II hypersensitivity can cause cellular dysfunction without cell lysis. (True)
E. Transfusion reactions are an example of Type II hypersensitivity. (True)

6. Explanation:

   • Type II hypersensitivity involves opsonization and phagocytosis of target cells.

   • Goodpasture syndrome and transfusion reactions are examples of Type II hypersensitivity.

   • Type II hypersensitivity is mediated by IgG or IgM, not IgE antibodies.

   • Antibodies in Type II hypersensitivity can cause cellular dysfunction (e.g., myasthenia gravis) without cell lysis.

6. Regarding Type III hypersensitivity:
   A. Type III hypersensitivity involves the formation of immune complexes in the circulation.
   B. Immune complexes in Type III hypersensitivity can deposit in the kidneys and joints.
   C. Type III hypersensitivity is mediated by T cells.
   D. Serum sickness is an example of Type III hypersensitivity.
   E. Type III hypersensitivity reactions are always systemic.

6. A. Type III hypersensitivity involves the formation of immune complexes in the circulation. (True)
   B. Immune complexes in Type III hypersensitivity can deposit in the kidneys and joints. (True)
   C. Type III hypersensitivity is mediated by T cells. (False)
   D. Serum sickness is an example of Type III hypersensitivity. (True)
   E. Type III hypersensitivity reactions are always systemic. (False)

   Explanation:

   • Type III hypersensitivity involves the formation of immune complexes that can deposit in tissues like the kidneys and joints.

   • Serum sickness is an example of Type III hypersensitivity.

   • Type III hypersensitivity is mediated by immune complexes, not T cells.

   • Type III reactions can be systemic (e.g., SLE) or localized (e.g., Arthus reaction).

6. Regarding Type IV hypersensitivity:
   A. Type IV hypersensitivity is also known as delayed-type hypersensitivity (DTH).
   B. Type IV hypersensitivity involves the activation of CD8+ cytotoxic T cells.
   C. Type IV hypersensitivity reactions occur within minutes of antigen exposure.
   D. Contact dermatitis is an example of Type IV hypersensitivity.
   E. Type IV hypersensitivity is mediated by antibodies.

6. Explanation:

   • Type IV hypersensitivity is also known as delayed-type hypersensitivity (DTH).

   • It involves the activation of CD8+ cytotoxic T cells and CD4+ T cells.

   • Type IV reactions are delayed, occurring 24-48 hours after antigen exposure.

   • Contact dermatitis is an example of Type IV hypersensitivity.

   • Type IV hypersensitivity is mediated by T cells, not antibodies.

Regarding hypersensitivity reactions in general:
A. Type I hypersensitivity is the only type that involves mast cell degranulation.
B. Type II hypersensitivity can lead to complement-mediated cell lysis.
C. Type III hypersensitivity involves the deposition of immune complexes in tissues.
D. Type IV hypersensitivity is mediated by B cells.
E. All hypersensitivity reactions involve the activation of the complement system.

A. Type I hypersensitivity is the only type that involves mast cell degranulation. (True)
B. Type II hypersensitivity can lead to complement-mediated cell lysis. (True)
C. Type III hypersensitivity involves the deposition of immune complexes in tissues. (True)
D. Type IV hypersensitivity is mediated by B cells. (False)
E. All hypersensitivity reactions involve the activation of the complement system. (False)

Explanation:

• Type I hypersensitivity is the only type that involves mast cell degranulation.

• Type II hypersensitivity can lead to complement-mediated cell lysis.

• Type III hypersensitivity involves immune complex deposition in tissues.

• Type IV hypersensitivity is mediated by T cells, not B cells.

• Not all hypersensitivity reactions involve complement activation (e.g., Type IV does not).

1. What is the primary mechanism of Type I hypersensitivity?
   .

1. Answer: Type I hypersensitivity is mediated by IgE antibodies, which bind to mast cells. Upon re-exposure to the allergen, the allergen binds to IgE, causing mast cell degranulation and the release of mediators like histamine, leading to rapid inflammation and tissue damage.
   Explanation: Type I hypersensitivity is characterized by a rapid response (within minutes) due to mast cell activation and the release of inflammatory mediators

1. What is the difference between Type II and Type III hypersensitivity?
   

1. Answer:

   • Type II Hypersensitivity: Mediated by IgG or IgM antibodies that target cell surface antigens, leading to cell lysis or dysfunction through opsonization, complement activation, or receptor blockade.

   • Type III Hypersensitivity: Involves the deposition of antigen-antibody complexes in tissues, leading to complement activation, inflammation, and tissue damage.
     Explanation: Type II involves direct antibody-mediated cell damage, while Type III involves immune complex deposition and subsequent inflammation.

1. What is the role of T cells in Type IV hypersensitivity?
   

1. Answer: In Type IV hypersensitivity, T cells (CD4+ and CD8+) mediate tissue damage. CD4+ T cells secrete cytokines, recruiting macrophages and causing inflammation (delayed-type hypersensitivity), while CD8+ T cells directly kill target cells (cytotoxic T cell-mediated reactions).
   Explanation: Type IV hypersensitivity is a cell-mediated reaction, with T cells playing a central role in inflammation and cytotoxicity.

1. What is the clinical significance of immune complex deposition in Type III hypersensitivity?
   

1. Answer: Immune complex deposition in Type III hypersensitivity leads to complement activation, recruitment of neutrophils, and inflammation, causing tissue damage. Common sites of deposition include the kidneys, joints, and blood vessels, leading to diseases like systemic lupus erythematosus (SLE) and post-streptococcal glomerulonephritis.
   Explanation: Immune complex deposition triggers inflammation and tissue injury, contributing to the pathogenesis of diseases like SLE and glomerulonephritis

1. What are the key differences between Type I and Type IV hypersensitivity?
   

1. Answer:

   • Type I Hypersensitivity: Mediated by IgE antibodies and mast cells, causing rapid reactions (within minutes). Examples include anaphylaxis and asthma.

   • Type IV Hypersensitivity: Mediated by T cells, causing delayed reactions (24-48 hours). Examples include tuberculosis and contact dermatitis.
     Explanation: Type I is antibody-mediated and rapid, while Type IV is cell-mediated and delayed.