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Chapter 65: Hypersensitivity (Allergy)

INTRODUCTION

Hypersensitivity reactions are exaggerated or inappropriate immune responses to benign antigens. It is the immune response, not the antigens, that is harmful to the host. Usually, hypersensitivity reactions occur in response to external, or “non-self,” antigens (covered in this chapter), whereas autoimmune reactions (see Chapter 66) occur in response to internal, or “self,” antigens.

Hypersensitivity reactions are antigen-specific, meaning that the first contact with the antigen sensitizes the immune system (i.e., primes the adaptive immune system), and subsequent contacts elicit the hypersensitive (allergic) response. Within an individual, these subsequent antigen exposures elicit similar clinical manifestations, although the severity of the hypersensitivity reactions may increase with time.

Hypersensitivity reactions can be subdivided into four main types. Types I, II, and III are antibody-mediated, whereas type IV is cell–mediated (Table 65–1). The immunologic reactions are summarized in Table 65–1. The clinical manifestations of the hypersensitivity reactions are described in Table 65–2.

TABLE 65–1Immunologic Aspects of Hypersensitivity Reactions
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TABLE 65–1 Immunologic Aspects of Hypersensitivity Reactions
Type Sensitization Immunologic Reaction

I (Immediate, anaphylactic)

IgE-mediated

 Antigen (allergen) induces IgE antibody that binds to mast cells and basophils. When exposed to the allergen again, the allergen cross-links the bound IgE on those cells. This causes degranulation and release of mediators (e.g., histamine).

II (Cytotoxic)

IgG-mediated

 Antigens on a cell surface elicit Tfh and B-cell activation. Antibody binding to cell membrane antigens leads to complement-mediated lysis of the cells (e.g., transfusion or Rh reactions) or autoimmune hemolytic anemia.

III (Immune complex)

Multiple types of antibodies

 Soluble antigens elicit Tfh and B-cell activation. Antigen–antibody immune complexes are deposited in tissues and neutrophils are attracted to the site. They release lysosomal enzymes, causing tissue damage. In the case of IgM or IgG, complement is also involved.

IV (Delayed)

T-cell–mediated

 CD4 and/or CD8 T cells sensitized by protein antigens. Memory T cells release cytokines upon second contact with the same antigen. The lymphokines induce inflammation and activate macrophages, which, in turn, release various inflammatory mediators.

Tfh = T follicular helper cell.

TABLE 65–2Clinical Manifestations of Hypersensitivity Reactions
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TABLE 65–2 Clinical Manifestations of Hypersensitivity Reactions
Type Typical Time of Onset Clinical Manifestation or Disease
I (Immediate, anaphylactic) Minutes Systemic anaphylaxis, urticaria (hives), asthma, hay fever, allergic rhinitis, allergic conjunctivitis, atopic dermatitis (eczema), angioedema; allergies to foreign substances such as food (e.g., nuts, shellfish, eggs), pollen, penicillin, bee venom, or latex gloves
II (Cytotoxic) Hours to days Hemolytic anemia, neutropenia, thrombocytopenia, ABO transfusion reactions, Rh incompatibility (erythroblastosis fetalis, hemolytic disease of the newborn), rheumatic fever, Goodpasture’s syndrome
III (Immune complex) 2–3 weeks Systemic lupus erythematosus, rheumatoid arthritis, poststreptococcal glomerulonephritis, IgA nephropathy, serum sickness, hypersensitivity pneumonitis (e.g., farmer’s lung)
IV (Delayed) 2–3 days Contact dermatitis, poison oak/ivy, tuberculin skin test reaction, drug rash, Stevens-Johnson syndrome, toxic epidermal necrolysis, erythema multiforme
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