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Artificial Antigen Presenting Cell (aAPC) Mediated Activation and Expansion of Natural Killer T Cells
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Artificial Antigen Presenting Cell (aAPC) Mediated Activation and Expansion of Natural Killer T Cells

Published on: December 29, 2012

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

J C Waldrep, H J Kaplan

    Investigative Ophthalmology & Visual Science
    |October 1, 1983
    PubMed

    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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