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Effect of tumor growth factor-beta on NK receptor expression by allostimulated CD8+ T lymphocytes
N Guerra1, K Benlhassan, G Carayol
1Unité INSERM U.487, PR1, Institut Gustave-Roussy, 39, rue Camille-Desmoulins, 94805 Villejuif Cedex, France.
We have examined the influence of the immunosuppressive cytokine TGF-beta on NK receptor expression by T lymphocytes upon allogeneic activation. Using the primary mixed lymphocyte reaction (MLR), our data show that allostimulation induced the expression of CD94/NKG2-A on alloactivated CD8+ T cells. This expression was increased in the presence of TGF-beta whereas IL-15 had no significant effect. The blockage of CD94 and NKG2-A resulted in increased lysis of targets by alloactivated cytotoxic T cells. This increase was dependent on the activation state of T cells. Using PCR, we also demonstrated that TGF-beta had no effect on the transcription of non-inhibitory NKG2 molecules. The present results show that allostimulation can induce CD94 and further point out the role of TGF-beta in the induction of the CD94/NKG2-A receptor on alloactivated T cells.
We have examined the influence of the immunosuppressive cytokine TGF-beta on NK receptor expression by T lymphocytes upon allogeneic activation. Using the primary mixed lymphocyte reaction (MLR), our data show that allostimulation induced the expression of CD94/NKG2-A on alloactivated CD8+ T cells. This expression was increased in the presence of TGF-beta whereas IL-15 had no significant effect. The blockage of CD94 and NKG2-A resulted in increased lysis of targets by alloactivated cytotoxic T cells. This increase was dependent on the activation state of T cells. Using PCR, we also demonstrated that TGF-beta had no effect on the transcription of non-inhibitory NKG2 molecules. The present results show that allostimulation can induce CD94 and further point out the role of TGF-beta in the induction of the CD94/NKG2-A receptor on alloactivated T cells.