DTH to allogeneic histocompatibility antigens is a T cell dependent reaction, which can be induced in immunologically competent individuals by subcutaneous (s.c.) or intravenous (i.v.) administration of alloantigens (Vander Kwast and Benner, 1978; Bianchi et al., 1984). After immunization, activated antigen-specific T cells and, possibly, T cell derived factors circulate through the body and mediate an effective immune-surveillance. After reencounter with the specific antigen, for example after injection of the relevant allogeneic spleen cells into a hind foot, these T cells or their factors cause the release of vasoactive substances, which lead to the accumulation of granulocytes, mononuclear cells and edemic fluid. This inflammatory response appears as a swelling of the site of reencounter of the antigen, which is maximal between 24 and 96 hours after antigen administration. The delayed onset distinguishes DTH from the more immediate types of hypersensitivity. DTH can also be induced in immunologically incompetent individuals, by the infusion of allogeneic, immunocompetent T cells. This leads to a state of DTH directed to the host histocompatibility antigens (Wolters and Benner, 1978). Anti-host DTH can be assayed by secondary transfer of lymphoid cells from the irradiated recipients to naive secondary recipients, syngeneic to the original spleen cell donors. The secondary recipients are subsequently challenged in a hind foot with spleen cells expressing the alloantigens of the primary irradiated recipients. The T cells that mediate DTH probably represent a subset of Th cells (Bianchi et al., 1981; Mossman and Coffman, 1987), although certain cloned Tc cells mediating DTH have been described (Lin and Askonas, 1981; Weiss and Dennert, 1981).

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Erasmus University Rotterdam
R. Benner (Robbert)
Stichting voor Medisch Onderzoek en Onderzoek en Gezondheidsonderzoek , Dutch Kidney Foundation
hdl.handle.net/1765/51190
Erasmus MC: University Medical Center Rotterdam

Molendijk, A. (1987, December 23). Suppressor cell mediated regulation of delayed-type hypersensitivity to histocompatibility antigens. Retrieved from http://hdl.handle.net/1765/51190