Cohen S B, Crawley J B, Kahan M C, Feldmann M, Foxwell B M
Mathilda and Terence Kennedy Institute of Rheumatology, UK.
Immunology. 1997 Sep;92(1):1-5. doi: 10.1046/j.1365-2567.1997.00348.x.
We demonstrate that interleukin-10 (IL-10) can inhibit T-cell apoptosis. T cells, within a PBMC (peripheral blood mononuclear cell) population, were stimulated via the T-cell receptor and grown in the presence of IL-2. These cells had less apoptosis when in the continuous presence of IL-10, compared with cells grown in the absence of IL-10. Conversely, when stimulated and grown in the presence of neutralizing antibody of IL-10, there was an increase in T-cell apoptosis. The in vitro rescue from apoptotic cell death of other lymphoid cells, such as germinal centre B cells, has been shown by others to involve a Bcl-2 pathway. We therefore investigated whether IL-10 might affect the Bcl-2 expression on cultured T cells. By Western blotting we demonstrated that continuous exposure of IL-10 to T cells (within a PBMC population) enhanced the expression of Bcl-2. Furthermore, T cells protected from apoptotic cell death by IL-10 were indistinguishable from viable untreated cells in their ability to proliferate to either immobilized anti-CD3 or IL-2. Thus, we have shown that continuous culture of T cells in the presence of IL-10 will inhibit T-cell apoptosis because of, at least in part, the upregulation of Bcl-2, and this is associated with a normal proliferative function.
我们证明白细胞介素-10（IL-10）可抑制T细胞凋亡。在外周血单个核细胞（PBMC）群体中的T细胞通过T细胞受体受到刺激，并在IL-2存在的情况下生长。与在无IL-10条件下生长的细胞相比，这些细胞在持续存在IL-10时凋亡较少。相反，当在IL-10中和抗体存在的情况下受到刺激并生长时，T细胞凋亡增加。其他人已表明，从其他淋巴细胞如生发中心B细胞的凋亡性细胞死亡中进行体外挽救涉及Bcl-2途径。因此，我们研究了IL-10是否可能影响培养的T细胞上Bcl-2的表达。通过蛋白质免疫印迹法，我们证明IL-10持续作用于（PBMC群体中的）T细胞可增强Bcl-2的表达。此外，受到IL-10保护免于凋亡性细胞死亡的T细胞在增殖至固定化抗CD3或IL-2的能力方面与未处理的活细胞没有区别。因此，我们已经表明，在IL-10存在的情况下持续培养T细胞将抑制T细胞凋亡，这至少部分是由于Bcl-2的上调，并且这与正常的增殖功能相关。
