Anterior chamber-associated immune deviation induced by TNP-splenocytes (TNP-ACAID). II. Suppressor T-cell networks.
Injection of trinitrophenyl (TNP)-modified splenocytes (TNP-Sp) into the anterior chamber (AC) of the eye results in systemic tolerance to TNP, a phenomenon termed "AC-associated immune deviation" or "TNP-ACAID". The systemic tolerance of TNP-ACAID is mediated by splenic suppressor T cells (Ts) that comprise an immunoregulatory network made up of two functionally distinct subsets (Ts-I and Ts-II). Ts-I is antigen-specific and cyclophosphamide (Cy)-sensitive, and requires a Cy-sensitive auxiliary cell. Conversely, Ts-II is antigen-nonspecific and Cy-resistant, and requires a TNP-derived accessory macrophage. Suppression via Ts-II is demonstrated only when Ts-I cells are inactivated functionally by Cy. Ts-II cells are regulated by T cells isolated from splenocytes containing active Ts-I suppressors. This contrasuppressive activity is mediated by Ts-I, or perhaps by a third T-cell subpopulation. The relationship between the two suppressor pathways in TNP-ACAID is discussed.
D000818:Animals; D000867:Anterior Chamber / Q000276:immunology*; D003520:Cyclophosphamide / Q000494:pharmacology; D008264:Macrophages / Q000276:immunology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D009578:Nitrobenzenes / Q000276:immunology*; D013154:Spleen / Q000276:immunology*; D050378:T-Lymphocytes, Regulatory / Q000276:immunology*; D014301:Trinitrobenzenes / Q000276:immunology*
D009578:Nitrobenzenes; D014301:Trinitrobenzenes; D003520:Cyclophosphamide