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antigen would instruct the genetically predisposed capability of into the tissues, and sometimes ischemic necrosis. Periarteritis multipotential cells as to which antibody to produce and might nodosa results from a similar antigen-antibody reaction and is also command the cells to proliferate, resulting in clones of prop- characterised by inflammation of the smaller arteries and periarte- erly instructed cells. rial structures. It is accompanied by proliferation of the intima There are two possible mechanisms for the elimination of anti- and two types of occlusion: (a) by proliferation or thrombosis; or bodies against self: immunological nonresponsiveness and (b) by the formation of nodules containing neutrophils and immunological paralysis. There are several states of immunologi- eosinophils. cal nonresponsivene: ne is illustrated by the exposure of a foe- tus or newborn to an antigen prior to the development of its ability | Anaphylaxis to recognise the antigen as non-self (immunological Injection of antigen and its combination with antibody may incompetence). Immunological paralysis results from the injec- cause release from the cells (especially mast-cell fixed basophils) tion of a very large amount of antigen into immunologically com- of physiologically active substances such as histamine, serotonin, petent individuals. Nonspecific immunological suppression by acetylcholine, slow-reacting substances (SRS) and heparin. They cortisone, ACTH, nitrogen mustards and irradiation is also well act on smooth muscle and blood vessels and cause anaphylactic known. (hypersensitivity) shock, asthma attack, allergic oedema, rhinitis Cellular sensitivity, also known as delayed or cellular hyper - _ or hay fever, and accumulation of fluid in the joints. sensitivity, depends on the development of immunologically reac- tive or "sensitive" lymphocytes and possibly other cells which Atopy react with the corresponding antigen to give a typical delayed- Atopy is caused by the union of antigen—usually pollens, dust, type reaction after a period of several hours, days or even weeks. milk, wheat and animal danders—with a peculiar type of antibody Cellular hypersensitivity depends on the original antigenic stim- (reagin). This reaction is relatively heat-labile and cannot be ulation and a latent period, and is demonstrated by in vitro procedure. It specific in its response. Delayed- has a special affinity for the skin and type hypersensitivity is characteristic for familial predisposition to the dis- of the body's response to various . ease. The reaction is nevertheless infectious agents such as viruses, The inflammatory response similar to other immediate-type sensi- bacteria, fungi, spirochetes and para- which occurs in delayed-type tivities, with the release of histamine sites. It is also characteristic of the and its manifestation principally as body's response to various chemi- hypersensitivity may not be asthma (breathing paralysis), hay cals, such as mercury, endotoxins, protective, and in many fever, urticaria, angioedema and antibiotics, various drugs and many . infantile eczema. other substances foreign to the body. instances may even be The induction of a hypersensitivity harmful Delayed Hypersensitivity reaction requires the presence in the tissues of the whole organism or cer- tain derivatives of it, in addition to the specific antigen such as a lipid, in The typical pathology of delayed hypersensitivity due to infectious agents involves perivascular infiltra- tion of lymphocytes and histiocytes addition to tubercle bacillus protein. Sensitisation to a non-infec- with the destruction of the antigen-containing parenchyma in the tious substance must be mediated through the skin or mucuous infiltrated area. The visual manifestations may vary from slight membranes which probably provide further necessary co-factors. erythema and oedema to a violent reaction with progressive tissue A delayed hypersensitivity reaction may be enhanced experi- destruction and necrosis. Local reactions include papular rose mentally by the employment of the antigen in a mineral oil adju- spots of typhoid fever, meningitis and a variety of infectious dis- vant with added Mycobacterium tuberculosis or by injection of eases, and contact sensitivities to plant and chemical substances the antigen directly into the lymphatics. The delayed hypersensi- manifesting as erythema, followed by papule and vesicle forma- tivity response is accompanied by mild to severe inflammation tion with resultant tissue damage and desquamation. Systemic which may cause cell injury and necrosis. The inflammatory reactions may accompany severe local reactions or may result response which occurs in delayed-type hypersensitivity may not from inhalation of the allergenic substances. be protective, and in many instances may even be harmful (e.g., Humoral antibodies do not seem to play a role in delayed rejection of grafts is directly linked to delayed hypersensitivity). hypersensitivity reaction. The reactivity is transferred only by cells, presumably sensitised lymphocytes, and it is unlikely that IMMUNOPATHOLOGY OF HYPERSENSITIVITY histamine or other physiologically active substances play a role in REACTIONS: the reaction. The reaction extends to any or all tissues where the Immediate Hypersensitivity offending antigen may occur. Ax 7 into the tissues, and sometimes ischemic necrosis. Periarteritis nodosa results from a similar antigen-antibody reaction and is characterised by inflammation of the smaller arteries and periarte- rial structures. It is accompanied by proliferation of the intima and two types of occlusion: (a) by proliferation or thrombosis; or (b) by the formation of nodules containing neutrophils and eosinophils. Anaphylaxis Injection of antigen and its combination with antibody may cause release from the cells (especially mast-cell fixed basophils) of physiologically active substances such as histamine, serotonin, acetylcholine, slow-reacting substances (SRS) and heparin. They act on smooth muscle and blood vessels and cause anaphylactic (hypersensitivity) shock, asthma attack, allergic oedema, rhinitis or hay fever, and accumulation of fluid in the joints. The inflammatory response which occurs in delayed-type hypersensitivity may not be protective, and in many instances may even be harmful. IMMUNOPATHOLOGY OF HYPERSENSITIVITY REACTIONS: Immediate Hypersensitivity This is the antibody-type reaction that is a secondary conse- quence to the beneficial effect of the combination of an antibody with its antigen. Isoimmunological Disease This is the result of an immunological reaction of a member of the same species to the tissue of another member of the same species. A blood transfusion reaction in a person given an incom- patible blood type is a typical example. Another example is ery- throblastosis fetalis, which results from the transfer of antibodies against the red blood cells of the foetus to the foetal circulation. Homograft rejection of tissues or organs between nonisologous members of a species is also immunologically based. Arthus-type Reaction This reaction results from the precipitative union of a large amount of antigen with a highly reactive antibody in the blood vessels, and leads to vascular damage. The cascade of events includes spastic contraction of the arterioles, endothelial damage, formation of leukocyte thrombi, exudation of fluid and blood cells 42 = NEXUS FEBRUARY —- MARCH 2001