Gilliet Michel, Liu Yong-Jun
Department of Immunology, DNAX Research Institute of Molecular and Cellular Biology, 901 California Avenue, Palo Alto, CA 94304, USA.
J Exp Med. 2002 Mar 18;195(6):695-704. doi: 10.1084/jem.20011603.
Although CD8 T cell-mediated immunosuppression has been a well-known phenomenon during the last three decades, the nature of primary CD8 T suppressor cells and the mechanism underlying their generation remain enigmatic. We demonstrated that naive CD8 T cells primed with allogeneic CD40 ligand-activated plasmacytoid dendritic cells (DC)2 differentiated into CD8 T cells that displayed poor secondary proliferative and cytolytic responses. By contrast, naive CD8 T cells primed with allogeneic CD40 ligand-activated monocyte-derived DCs (DC1) differentiated into CD8 T cells, which proliferated to secondary stimulation and killed allogeneic target cells. Unlike DC1-primed CD8 T cells that produced large amounts of interferon (IFN)-gamma upon restimulation, DC2-primed CD8 T cells produced significant amounts of interleukin (IL)-10, low IFN-gamma, and no IL-4, IL-5, nor transforming growth factor (TGF)-beta. The addition of anti-IL-10-neutralizing monoclonal antibodies during DC2 and CD8 T cell coculture, completely blocked the generation of IL-10-producing anergic CD8 T cells. IL-10-producing CD8 T cells strongly inhibit the allospecific proliferation of naive CD8 T cells to monocytes, and mature and immature DCs. This inhibition was mediated by IL-10, but not by TGF-beta. IL-10-producing CD8 T cells could inhibit the bystander proliferation of naive CD8 T cells, provided that they were restimulated nearby to produce IL-10. IL-10-producing CD8 T cells could not inhibit the proliferation of DC1-preactivated effector T cells. This study demonstrates that IL-10-producing CD8 T cells are regulatory T cells, which provides a cellular basis for the phenomenon of CD8 T cell-mediated immunosuppression and suggests a role for plasmacytoid DC2 in immunological tolerance.
尽管在过去三十年中,CD8 T细胞介导的免疫抑制一直是一个广为人知的现象,但原发性CD8 T抑制细胞的本质及其产生的机制仍然不明。我们证明,用同种异体CD40配体激活的浆细胞样树突状细胞(DC)2致敏的初始CD8 T细胞分化为对二次增殖和细胞溶解反应较差的CD8 T细胞。相比之下,用同种异体CD40配体激活的单核细胞衍生的树突状细胞(DC1)致敏的初始CD8 T细胞分化为CD8 T细胞,其在二次刺激下增殖并杀死同种异体靶细胞。与再次刺激时产生大量干扰素(IFN)-γ的DC1致敏的CD8 T细胞不同,DC2致敏的CD8 T细胞产生大量白细胞介素(IL)-10、低水平的IFN-γ,且不产生IL-4、IL-5或转化生长因子(TGF)-β。在DC2和CD8 T细胞共培养期间添加抗IL-10中和单克隆抗体,完全阻断了产生IL-10的无反应性CD8 T细胞的产生。产生IL-10的CD8 T细胞强烈抑制初始CD8 T细胞对单核细胞以及成熟和未成熟树突状细胞的同种异体特异性增殖。这种抑制是由IL-10介导的,而不是由TGF-β介导的。产生IL-10的CD8 T细胞可以抑制初始CD8 T细胞的旁观者增殖,前提是它们在附近被再次刺激以产生IL-10。产生IL-10的CD8 T细胞不能抑制DC1预激活的效应T细胞的增殖。这项研究表明,产生IL-10的CD8 T细胞是调节性T细胞,这为CD8 T细胞介导的免疫抑制现象提供了细胞基础,并提示浆细胞样DC2在免疫耐受中的作用。