Guerra N, Benlhassan K, Carayol G, Guillard M, Pardoux C, Chouaib S, Caignard A
Unité INSERM U.487, PR1, Institut Gustave-Roussy, 39, rue Camille-Desmoulins, 94805 Villejuif Cedex, France.
Eur Cytokine Netw. 1999 Sep;10(3):357-64.
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.
我们研究了免疫抑制细胞因子转化生长因子-β(TGF-β)对同种异体激活后T淋巴细胞NK受体表达的影响。利用原发性混合淋巴细胞反应(MLR),我们的数据表明同种异体刺激可诱导同种异体激活的CD8⁺T细胞上CD94/NKG2-A的表达。在TGF-β存在的情况下,这种表达会增加,而白细胞介素-15(IL-15)则没有显著影响。阻断CD94和NKG2-A会导致同种异体激活的细胞毒性T细胞对靶标的杀伤增加。这种增加取决于T细胞的激活状态。通过聚合酶链反应(PCR),我们还证明TGF-β对非抑制性NKG2分子的转录没有影响。目前的结果表明同种异体刺激可诱导CD94表达,并进一步指出TGF-β在同种异体激活的T细胞上诱导CD94/NKG2-A受体中的作用。