Skin Diseases with an Immune Component, Part I: Allergic and Hypersensitivity-Related Conditions

Editor-in-Chief: Nikki A. Levin, MD, PhD
Editor-in-Chief: Cathleen K. Case, MS, ANP-BC, DCNP
Medical Writer for original manuscript: Nancy J. Nordenson, MT (ASCP), MFA
Medical Writer for updates to manuscript: Joshua F. Kilbridge

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Introduction

A hypersensitivity reaction is an exaggerated and pathologic response by the immune system to a self- or foreign antigen.^1,2 Four types of hypersensitivity reactions are recognized², which differ in mediators involved, mechanisms, timing, and clinical manifestations (Table).^2-4

Table. Four Types of Hypersensitivity Reactions^2-4

Type	Mediators	Mechanism	Timing*	Examples of Conditions
Type I (immediate/ anaphylactic)	IgE, histamine, tryptase, leukotrienes	IgE, produced in excessive amounts, interacts with mast cells to cause release of histamine and other inflammatory compounds	15–30 min, usually; 10–12 h for some delayed reactions	Anaphylaxis, asthma, urticaria, angioedema
Type II (cytotoxic)	IgG or IgM, complement	Antibody is bound to antigen on cell surface, triggering complement activation, phagocytosis, and cytotoxicity	Minutes to hours	Some drug reactions, transfusion reactions
Type III (immune complex)	IgG or IgM immune complexes	Antigen-antibody immune complexes are deposited in tissue, activating mast cells, neutrophils, and phagocytes and triggering complement cascade	3–10 h	Serum sickness, arthus reaction, vasculitis, systemic lupus erythematosus
Type IV (delayed/ cell-mediated)	Antigen-specific T-cells; monocyte chemotactic factor, interleukin-2, interferon-gamma, TNF alpha and beta	Activated antigen-specific helper T-cells stimulate release of cytokines and chemokines, which attract and activate macrophages, eosinophils, and neutrophils; cytotoxic T-cells cause damage directly	1–3 d; up to 4 wk for some reactions	Allergic contact dermatitis, tuberculin reaction, granuloma formation

*Timing from exposure to antigen.