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Insulin-specific suppressor T cell factors.

P E Jensen, J A Kapp

    Journal of Immunology (Baltimore, Md. : 1950)
    |February 15, 1986
    PubMed
    Summary
    This summary is machine-generated.

    Murine antibody responses to insulin are controlled by immune response genes. Insulin-specific suppressor factors (TsF) from T cells replace suppressor cell activity, revealing that preferential suppressor T cell activation causes nonresponsiveness.

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    Area of Science:

    • Immunology
    • T cell regulation
    • MHC-restricted immune responses

    Background:

    • Murine antibody production to heterologous insulins is governed by MHC-linked immune response genes.
    • Nonresponder mice, despite lacking antibody response, possess radioresistant helper T cells activated by nonimmunogenic insulin variants.
    • Helper T cell activity is masked by radiosensitive suppressor T cells (Lyt-1-2+, I-J+).

    Purpose of the Study:

    • To investigate the nature of insulin-specific suppressor T cells (TsF) and their role in nonresponsiveness.
    • To characterize the molecular components and MHC restriction of insulin-specific TsF.
    • To elucidate the mechanism underlying the nonresponder phenotype in mice.

    Main Methods:

    • Extraction and in vitro functional analysis of insulin-specific suppressor factors (TsF) from primed T cells.

    Related Experiment Videos

  • Immunoadsorption studies to assess antigen binding and MHC determinant association.
  • Analysis of TsF subunit composition and function using isolated chains from different mouse strains.

    • Main Results:

    • Primed T cell extracts contain insulin-specific TsF that substitute for suppressor T cell activity in vitro.
    • TsF activity is MHC-linked, mapping to the I-J region, and TsF binds antigen.
    • Insulin-specific TsF comprises at least two chains: one for antigen binding and another bearing I-J determinants for MHC restriction.

    Conclusions:

    • The antigen-binding chain determines specificity, while the I-J+ chain dictates MHC restriction.
    • Reconstitution experiments show that TsF composed of antigen-binding chains from any strain and I-J+ chains from responder strains can activate responder lymphocytes.
    • Preferential activation of suppressor T cells, not differential sensitivity, is the likely cause of the nonresponder phenotype to insulin.