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Induction of CD4(+) T cell alloantigen-specific hyporesponsiveness by IL-10 and TGF-beta(1)

  1. Author:
    Zeller, J. C.
    Panoskaltsis-Mortari, A.
    Murphy, W. J.
    Ruscetti, F. W.
    Narula, S.
    Roncarolo, M. G.
    Blazar, B. R.

  2. Author Address

    Blazar BR Univ Minnesota Hosp & Clin Box 109 Mayo Bldg,420 SE Delaware St Minneapolis, MN 55455 USA Univ Minnesota, Ctr Canc, Dept Pediat, Div Bone Marrow Transplantat Minneapolis, MN 55455 USA SAIC Frederick Frederick, MD 21702 USA NCI, Lab Leukocyte Biol, Frederick Canc Res & Dev Ctr Frederick, MD 21702 USA Schering Plough Corp, Res Inst Kenilworth, NJ 07033 USA Telethon Inst Gene Therapy H San Raffaele Milan Italy
    1. Year: 1999
  2. Journal: Journal of Immunology
    1. 163
    2. 7
    3. Pages: 3684-3691
  4. Type of Article: Article
  1. Abstract:

    Induction and maintenance of Ag-specific tolerance are pivotal for immune homeostasis, prevention of autoimmune disorders, and the goal of transplantation. Recent studies suggest that certain cytokines, notably IL-10 and TGF-beta, may play a role in downregulating immune functions. To further examine the role of cytokines in Ag-specific hyporesponsiveness, murine CD4(+) T cells were exposed ex vivo to alloantigen-bearing stimulators in the presence of exogenous IL-10 and/or TGF-beta. Primary but not secondary alloantigen proliferative responses were inhibited by IL-10 alone. However, the combined addition of TL-10+ TGF-beta markedly induced alloantigen hyporesponsiveness in both primary and secondary MLR cultures. Alloantigen-specific hyporesponsiveness was observed also under conditions in which nominal Ag responses were intact, In adoptive transfer experiments, IL-10 + TGF-beta-treated CD4(+) T cells, but not T cells treated with either cytokine alone, mere markedly impaired in inducing graft-vs-host disease alloresponses to MHC class II disparate recipients. These data provide the first formal evidence that IL-10 and TGF-beta have at least an additive effect in inducing alloantigen-specific tolerance, and that in vitro cytokines can be exploited to suppress CD4(+) T cell-mediated Ag-specific responses in vivo. [References: 41]

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