Hypersensitivity Types I-IV Review

A comprehensive set of practice questions covering the definitions, mechanisms, mediators, and clinical examples of Type I, II, III, and IV hypersensitivity reactions based on the lecture transcript.

What is the definition of hypersensitivity according to the lecture?

Hypersensitivity refers to over-reactions of the immune system to harmless antigens, resulting in a heightened and exaggerated immune response that can cause tissue damage, disease, or death.

What is an allergen?

An allergen is an environmental antigen that induces a state of hypersensitivity (or allergy).

What is the immune reactant and typical onset time for Type I hypersensitivity?

The immune reactant is $IgE$ antibodies, and the reaction is very rapid, typically occurring within $30\,minutes$ of encounter, earning it the name "immediate" hypersensitivity.

Distinguish between systemic and local atopic reactions in Type I hypersensitivity.

A systemic atopic response is anaphylaxis which affects the entire body, while local atopic reactions (like allergic rhinitis, asthma, or eczema) are generally confined to the anatomical location of the affected tissue.

What are the primary mediators released during mast cell degranulation in Type I hypersensitivity?

Primary mediators include histamine (causes vasodilation and increased vascular permeability), leukotrienes, and prostaglandins (contribute to inflammation and smooth muscle contraction).

What are the immune reactants for Type II hypersensitivity, and what is its common name?

The immune reactants are $IgG$ or $IgM$ antibodies, and it is also known as a cytotoxic reaction.

List the three mechanisms of cell killing in Type II hypersensitivity.

1. Complement mediated cell lysis. 2. Antibody dependent cell mediated cytotoxicity (ADCC). 3. Opsonization (leading to phagocytosis).

What is Antibody-Mediated Cellular Dysfunction in the context of Type II hypersensitivity?

It occurs when autoantibodies bind to cell-surface receptors and impair or dysregulate cell function without causing cell injury or inflammation, such as in Myasthenia gravis (blocking $ACh$ receptors) or Graves' disease (stimulating $TSH$ receptors).

How does Type III hypersensitivity differ from Type II in terms of antigen type?

Type III involves soluble antigens that form immune complexes, whereas Type II involves antigens that are cell- or matrix-associated (cell-bound).

What is the pathophysiological mechanism of Type III hypersensitivity?

Accumulation of antigen-antibody (immune) complexes precipitate in tissues (like skin, joints, or vessels), triggering the classical complement pathway, which recruits neutrophils that release lysosomal enzymes and free radicals, causing tissue damage.

Provide three examples of Type III hypersensitivity diseases.

Systemic Lupus Erythematosus (SLE), Rheumatoid Arthritis, and Serum Sickness.

What is the characteristic timing and mediator for Type IV hypersensitivity?

Type IV is mediated by $T$ cells ($Th1$, $Th2$, or $CTL$) and is known as delayed-type hypersensitivity (DTH) because it reaches a peak level within $48-72\,hours$ after the second encounter with the antigen.

What cells are the principal effector cells of the DTH (Type IV) response?

Macrophages are the principal effector cells, which are attracted and activated by cytokines and chemokines secreted by sensitized $T$ helper ($Th1$) cells.

Explain the Tuberculin Skin Test (Mantoux test) as an example of Type IV hypersensitivity.

A purified protein derivative (PPD) of tubercle bacilli is injected intradermally; if memory $Th1$ cells are present from prior exposure, they mount a response within $48-72\,hours$, resulting in a raised bump (induration) due to macrophage influx.

What is a hapten in the context of contact dermatitis?

A hapten is a small molecule that is not immunogenic on its own but becomes so when it binds to a larger carrier protein, usually within the body, to form a neo-antigen.