Hypersensitivity Types I and II

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Questions and Answers

During a Type I hypersensitivity reaction, which effector cell is primarily responsible for releasing histamine, leading to symptoms like wheal and flare?

  • Macrophage
  • Mast cell (correct)
  • T-helper 1 cell
  • Neutrophil

What is the primary mechanism by which Type II hypersensitivity reactions cause cellular damage?

  • IgE-mediated degranulation of mast cells.
  • T-cell mediated cytotoxicity.
  • Antibody-dependent cell-mediated cytotoxicity. (correct)
  • Immune complex formation leading to complement activation.

Which antibody class is predominantly involved in Type III hypersensitivity reactions?

  • IgD
  • IgG or IgM (correct)
  • IgE
  • IgA

In Type IV hypersensitivity reactions, what is the role of T-helper 1 cells?

<p>Releasing cytokines to recruit more T-helper cells and activate macrophages. (A)</p> Signup and view all the answers

Which hypersensitivity type is characterized by the formation of granulomas due to the accumulation of immune cells?

<p>Type III (C)</p> Signup and view all the answers

Why is a sudden drop in blood pressure a major concern in anaphylaxis?

<p>Due to vasodilation caused by histamine release. (A)</p> Signup and view all the answers

What immunological process underlies Hemolytic Disease of the Newborn (Erythroblastosis fetalis)?

<p>Maternal IgG antibodies against fetal red blood cell antigens. (A)</p> Signup and view all the answers

Why is Type IV hypersensitivity also known as delayed-type hypersensitivity?

<p>Because the reaction takes several days to develop, involving T-cell activation and cytokine production. (A)</p> Signup and view all the answers

Which of the following best describes the Arthus reaction, a localized form of Type III hypersensitivity?

<p>Recruitment of neutrophils and subsequent inflammation at the site of antigen injection. (D)</p> Signup and view all the answers

A patient presents with skin rashes, potentially diagnosed as Stevens-Johnson Syndrome (SJS). Which type of hypersensitivity is most likely involved in this condition?

<p>Type IV (D)</p> Signup and view all the answers

Flashcards

Type I Hypersensitivity

Involves IgE antibodies, mast cells, and basophils, leading to degranulation and release of histamine, causing reactions like anaphylaxis, wheal and flare, sneezing, and itchiness.

Type II Hypersensitivity

IgG or IgM antibodies mediate cytotoxic reactions, targeting cells. Examples include hemolytic anemia, blood transfusion reactions, Hemolytic Disease of the Newborn, and drug allergies.

Type III Hypersensitivity

IgG or IgM antibodies form immune complexes, activating complement (C3b), leading to neutrophil infiltration and granuloma formation. Examples include Systemic Lupus Erythematosus, Rheumatoid Arthritis and Serum sickness.

Type IV Hypersensitivity

T-cell mediated delayed hypersensitivity involving macrophages and T-helper 1 cells, causing inflammation. Examples include rashes, contact dermatitis (e.g., poison ivy), tubercular lesions, and graft rejection.

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Anaphylaxis

A potentially life-threatening reaction with a sudden drop in blood pressure; a Type I hypersensitivity reaction.

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Wheal and Flare Reaction

A swelling and redness of the skin; a common symptom of Type I hypersensitivity.

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Granuloma

Cluster of immune cells forming in response to chronic infection or inflammation.

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Arthus reaction

A hypersensitivity reaction involving recruitment of neutrophils.

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Study Notes

Type I Hypersensitivity

  • IgE antibody is involved in this type of reaction.
  • Mast cells, or basophils when in tissues, act as effector cells, and are characterized by a bilobed nucleus and large pores with blue-black granules.
  • Degranulation of the effector cell occurs, releasing components like serotonin (a vasoconstricting agent), heparin (a natural anticoagulant), and histamine as the major component.
  • A key characteristic is anaphylaxis, also known as anaphylactic shock, which involves a sudden drop in blood pressure and is life-threatening.
  • Reactions manifest as wheal and flare (swelling and redness of the skin), sneezing, and itchiness (pruritis).
  • It represents the allergic reaction most familiar to the general public.
  • The allergen binds to the Fab/Paratope region of the antibody, while the effector cell binds to the Fc region.
  • Examples include asthma, food allergy, hay fever, hives, and eczema.

Type II Hypersensitivity

  • IgG or IgM antibodies are involved, and it is also known as the cytotoxic type.
  • Examples of this type include hemolytic anemia, reactions to blood transfusions and Hemolytic Disease of the Newborn, also known as Erythroblastosis fetalis.
  • Also reactions to certain drugs, Hemoglobinuria (red urine), and Hemoglobinemia (pink coloration of plasma)

Type III Hypersensitivity

  • IgG or IgM antibodies are involved.
  • C3b, a complement protein also known as an immune complex, is involved.
  • Granulomas (clusters of immune cells) form in response to infection or inflammation.
  • Characterized by significant infiltration of neutrophils.
  • Examples include Systemic Lupus Erythematosus, Rheumatoid Arthritis, and Serum sickness (reaction to serum/vaccination).
  • Further examples are necrotizing vasculitis, glomerulonephritis, and Arthus reaction (recruitment of neutrophils).

Type IV Hypersensitivity

  • Known as delayed hypersensitivity.
  • Involves inflammatory, APC, and phagocytic cells, leading to significant inflammation.
  • Macrophages act as effector cells, releasing cytokines to signal T-helper 1 cells.
  • T-helper 1 cells release cytokines to recruit more T-helper cells.
  • Examples include rashes, Stevens-Johnson Syndrome (SJS), and contact dermatitis (e.g., poison ivy).
  • Further examples are tubercular lesions, graft rejection, and reactions to skin susceptibility tests such as the tuberculin skin test.

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