In medicine, hypersensitivity is an immune system disease that is defined as "altered reactivity to an antigen, which can result in pathologic reactions upon subsequent exposure to that particular antigen.."[1]
The four-group Gell and Coombs classification of immune reactions was proposed in 1963.[2]
Type 1 hypersensitivity is defined as "hypersensitivity reactions which occur within minutes of exposure to challenging antigen due to the release of histamine which follows the antigen-antibody reaction and causes smooth muscle contraction and increased vascular permeability."[3]
Examples include allergic asthma, allergic conjunctivitis, allergic rhinitis ("hay fever"), anaphylaxis, angioedema, eosinophilia, and urticaria (hives).
In type 2 hypersensitivity, the antibodies produced by the immune response bind to antigens on the patient's own cell surfaces. The antigens recognized in this way may either be intrinsic ("self" antigen, innately part of the patient's cells) or extrinsic (absorbed onto the cells during exposure to some foreign antigen, possibly as part of infection with a pathogen). These cells are recognised by macrophages or dendritic cells which act as antigen presenting cells, this causes a B cell response where antibodies are produced against the foreign antigen.
An example here is the reaction to penicillin where the drug can bind to red blood cells causing them to be recognised as different, B cell proliferation will take place and antibodies to the drug are produced. IgG and IgM antibodies bind to these antigens to form complexes that activate the classical pathway of complement activation for eliminating cells presenting foreign antigens (which are usually, but not in this case, pathogens). That is, mediators of acute inflammation are generated at the site and membrane attack complexes cause cell lysis and death. The reaction takes hours to a day.
Another form of type 2 hypersensitivity is called antibody-dependent cell-mediated cytotoxicity (ADCC). Here, cells exhibiting the foreign antigen are tagged with antibodies (IgG or IgM). These tagged cells are then recognised by natural killer (NK) cells and macrophages (recognised via IgG bound (via the Fc region) to the effector cell surface receptor, CD16 (FcγRIII)), which in turn kill these tagged cells.
Some examples:
Type 3 hypersensitivity occurs when antigens and antibodies are present in roughly equal amounts, causing extensive cross-linking. Large immune complexes that cannot be cleared are deposited in vessel walls and induce an inflammatory response. The reaction can take hours, days, or even weeks to develop.
Some clinical examples:
Type 4 hypersensitivity is often called delayed type as the reaction takes two to three days to develop. Unlike the other types of hypersensitivity, it is mediated by T-cells rather than B-cells.
Type 4 reactions can be subdivided by the specific type of T-cell response that occurs when macrophages present antigen in a complex with either type 1 or 2 major histocompatibility complex.[4]
Some clinical examples:
This is an additional type that is sometimes (often in Britain) used as a distinction from Type 2.[5]
Instead of binding to cell surface components, the antibodies recognize and bind to the cell surface receptors, which either prevents the intended ligand binding with the receptor or mimics the effects of the ligand, thus impairing cell signalling.
Some clinical examples: