Cyclophosphamide-sensitive contrasuppression in TNP-anterior chamber associated immune deviation (TNP-ACAID).
Injection of trinitrophenyl (TNP)-modified splenocytes (TNP-Sp) into the anterior chamber of the eye results in systemic tolerance to TNP, a phenomenon termed anterior chamber associated immune deviation (TNP-ACAID). Two distinct suppressor pathways develop after the induction of TNP-ACAID. The primary suppressor pathway (I) is antigen-specific, is mediated by a cyclophosphamide (Cy)-sensitive suppressor T cell (Ts-I), and requires a Cy-sensitive auxillary cell. The secondary suppressor pathway (II) is antigen nonspecific, is mediated by a Cy-resistant suppressor T cell (Ts-II), and requires a TNP-pulsed accessory macrophage. Suppression via pathway II is demonstrable only when Ts-I cells are functionally inactivated by Cy. Furthermore, the addition of T cells from Sp containing active Ts-I inhibits Ts-II. This suppression of a suppressor cell (i.e., contrasuppression) is mediated by either Ts-I or a third T cell population, which is also Cy sensitive.
D000818:Animals; D000867:Anterior Chamber / Q000276:immunology*; D003520:Cyclophosphamide / Q000008:administration & dosage*; D000939:Epitopes; D007108:Immune Tolerance; D007111:Immunity, Cellular / Q000187:drug effects; D007116:Immunization, Passive; D008264:Macrophages / Q000276:immunology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D013154:Spleen / Q000166:cytology; D050378:T-Lymphocytes, Regulatory / Q000145:classification* / Q000187:drug effects / Q000276:immunology; D014301:Trinitrobenzenes / Q000276:immunology
D000939:Epitopes; D014301:Trinitrobenzenes; D003520:Cyclophosphamide