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Investigative Ophthalmology & Visual Science, Vol 24, 1339-1345, Copyright © 1983 by Association for Research in Vision and Ophthalmology


ARTICLES AND REPORTS

Anterior chamber-associated immune deviation induced by TNP-splenocytes (TNP-ACAID). II. Suppressor T-cell networks

JC Waldrep and HJ Kaplan

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.





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Copyright © 1983 by the Association for Research in Vision and Ophthalmology