Toes R E, Schoenberger S P, van der Voort E I, Offringa R, Melief C J
Department of Immunohematology and Blood Bank, University Hospital Leiden, Leiden, AZ, 2333, The Netherlands.
Semin Immunol. 1998 Dec;10(6):443-8. doi: 10.1006/smim.1998.0147.
Tumor-specific immunity relies on interactions with the antigen receptors as well as costimulatory molecules, such as those of the CD28/B7 pathway and relatives of the TNFR gene family. Cytotoxic T lymphocytes specific for cellular antigens are in general primed by professional antigen-presenting cells that indirectly present antigens derived from cells in the periphery. This cross-priming of CD8(+) T cells requires signals provided by CD4(+) T helper cells. Although this dependency on [help' for efficient cytotoxic T lymphocyte priming has been well documented, it was only recently that more mechanistic insight into the nature of this event has been obtained. In the absence of the CD4(+) T cells, signalling through CD40 can replace 'help' required for priming of these CD8(+) T cells. These observations indicate that T cell help for cytotoxic T lymphocytes is mediated by CD40-CD40Ligand (L) interactions, most likely through activation of professional antigen-presenting cells that cross-present cellular antigens to these T cells.
肿瘤特异性免疫依赖于与抗原受体以及共刺激分子的相互作用，例如CD28/B7途径的分子和肿瘤坏死因子受体（TNFR）基因家族的相关分子。针对细胞抗原的细胞毒性T淋巴细胞通常由专职抗原呈递细胞致敏，这些专职抗原呈递细胞间接呈递来自外周细胞的抗原。CD8(+) T细胞的这种交叉致敏需要CD4(+) T辅助细胞提供信号。尽管对有效细胞毒性T淋巴细胞致敏所需“辅助”的这种依赖性已有充分记录，但直到最近才对这一事件的本质有了更多的机制性认识。在没有CD4(+) T细胞的情况下，通过CD40的信号传导可以替代这些CD8(+) T细胞致敏所需的“辅助”。这些观察结果表明，细胞毒性T淋巴细胞的T细胞辅助是由CD40- CD40配体（L）相互作用介导的，很可能是通过激活将细胞抗原交叉呈递给这些T细胞的专职抗原呈递细胞来实现的。
