IIIhypersensitivitet

Hypersensitivity refers to an exaggerated or inappropriate immune response to an antigen that would normally be harmless. This means the immune system overreacts to a substance that does not pose a threat, leading to tissue damage and disease. Hypersensitivity reactions are classified into four main types based on their underlying mechanisms, as described by Gell and Coombs.

Type I hypersensitivity, also known as immediate hypersensitivity or allergy, involves IgE antibodies. Upon initial exposure to an allergen, the immune system produces IgE antibodies. These antibodies then bind to mast cells and basophils. Upon re-exposure, the allergen cross-links the IgE on these cells, triggering the release of inflammatory mediators like histamine, leading to symptoms such as hives, asthma, and anaphylaxis.

Type II hypersensitivity, or cytotoxic hypersensitivity, involves IgG or IgM antibodies that bind to antigens on the surface of cells or in the extracellular matrix. This binding can lead to the destruction of the cells by complement activation or antibody-dependent cell-mediated cytotoxicity. Examples include transfusion reactions and hemolytic disease of the newborn.

Type III hypersensitivity, immune complex-mediated hypersensitivity, occurs when soluble antigens react with antibodies, forming immune complexes. These complexes can deposit in tissues, activating the complement system and attracting neutrophils, which release enzymes that damage the surrounding tissue. Systemic lupus erythematosus and serum sickness are examples of type III reactions.

Type IV hypersensitivity, delayed-type hypersensitivity, is cell-mediated and involves T lymphocytes, specifically T helper cells and cytotoxic T cells. It typically manifests 24-72 hours after exposure to an antigen. Examples include contact dermatitis from poison ivy and the tuberculin skin test reaction. These reactions are characterized by inflammation and tissue damage mediated by activated macrophages and cytotoxic T cells.