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Pathology - Hypersensitivity reactions
Definition • A collection of disorders resulting from an aberrant immune-mediated response. • This response may target an exogenous antigen from the environment or a self-antigen, in which case it constitutes a kind of autoimmunity.
Type 1 hypersensitivity
• Defined by the synthesis of IgE antibodies in reaction to an antigen. • The cross-linking of surface IgE receptors on mast cells triggers the release of mediators, including histamine, which incite acute inflammation. • Characteristic of individuals with atopy, a hereditary predisposition to generate elevated levels of IgE in reaction to environmental antigens such as pollen and house dust mites. Anaphylaxis is a systemic type of acute hypersensitivity resulting from the extensive release of histamine. In its most extreme manifestation, it may result in anaphylactic shock. • Immediate hypersensitivity disorders impact over 20% of the population, and their prevalence is increasing.
Antibody-mediated (type 2) hypersensitivity is induced by IgG or IgM antibodies attaching to a fixed antigen within a tissue. The binding of antibodies can activate the complement system, resulting in cellular damage, as seen in bullous pemphigoid or induce alterations in cellular function, exemplified by TSH-receptor stimulating antibodies in Graves' disease.
Immune complex-mediated (type 3) hypersensitivity • Arises from circulating IgG or IgM antibodies that form immune complexes with antigens in the bloodstream, subsequently depositing in tissues and activating complement. • Preferred sites for immune complex deposition include small blood vessels, kidneys, and joints. • Reactions characterized by immune complex-mediated hypersensitivity often manifest as multisystem disorders, prominently featuring vasculitis, arthritis, and glomerulonephritis, as observed in systemic lupus erythematosus.
T-cell-mediated (type 4) hypersensitivity is induced by activated T-lymphocytes that damage cells through direct cytotoxicity or by secreting cytokines that stimulate macrophage activation. • T-cell responses are characterized by a latency of 1–2 days, hence the designation delayed-type hypersensitivity. • Illustrative cases encompass contact dermatitisHashimoto’s thyroiditis primary biliary cirrhosisand tuberculosis.
Definition • A collection of disorders resulting from an aberrant immune-mediated response. • This response may target an exogenous antigen from the environment or a self-antigen, in which case it constitutes a kind of autoimmunity.
Type 1 hypersensitivity
• Defined by the synthesis of IgE antibodies in reaction to an antigen. • The cross-linking of surface IgE receptors on mast cells triggers the release of mediators, including histamine, which incite acute inflammation. • Characteristic of individuals with atopy, a hereditary predisposition to generate elevated levels of IgE in reaction to environmental antigens such as pollen and house dust mites. Anaphylaxis is a systemic type of acute hypersensitivity resulting from the extensive release of histamine. In its most extreme manifestation, it may result in anaphylactic shock. • Immediate hypersensitivity disorders impact over 20% of the population, and their prevalence is increasing.
Antibody-mediated (type 2) hypersensitivity is induced by IgG or IgM antibodies attaching to a fixed antigen within a tissue. The binding of antibodies can activate the complement system, resulting in cellular damage, as seen in bullous pemphigoid or induce alterations in cellular function, exemplified by TSH-receptor stimulating antibodies in Graves' disease.
Immune complex-mediated (type 3) hypersensitivity • Arises from circulating IgG or IgM antibodies that form immune complexes with antigens in the bloodstream, subsequently depositing in tissues and activating complement. • Preferred sites for immune complex deposition include small blood vessels, kidneys, and joints. • Reactions characterized by immune complex-mediated hypersensitivity often manifest as multisystem disorders, prominently featuring vasculitis, arthritis, and glomerulonephritis, as observed in systemic lupus erythematosus.
T-cell-mediated (type 4) hypersensitivity is induced by activated T-lymphocytes that damage cells through direct cytotoxicity or by secreting cytokines that stimulate macrophage activation. • T-cell responses are characterized by a latency of 1–2 days, hence the designation delayed-type hypersensitivity. • Illustrative cases encompass contact dermatitisHashimoto’s thyroiditis primary biliary cirrhosisand tuberculosis.
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