Cyclophosphamide-sensitive contrasuppression in TNP-anterior chamber associated immune deviation (TNP-ACAID).
Open Access
- 1 December 1983
- journal article
- research article
- Published by Oxford University Press (OUP) in The Journal of Immunology
- Vol. 131 (6) , 2746-2750
- https://doi.org/10.4049/jimmunol.131.6.2746
Abstract
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.This publication has 18 references indexed in Scilit:
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