中文摘要：

局部免疫抑制经iC3b—Mo／Mph-丝裂原活化蛋白激酶信号传导途径，诱导细胞外信号调节激酶p44／42磷酸化，产生高水平的IL-10，促进单核巨噬细胞朝巨噬细胞的方向发展，以吞噬uV暴露部位的坏死细胞。同时抑制磷酸化p38丝裂原活化蛋白激酶和IL-12的产生，阻碍单核巨噬细胞向CDIc＋树突细胞方向分化和成熟，以抑制T细胞主导的免疫反应。在UV引起的系统性免疫抑制中，其机制并非通过直接抑制DC的数量和功能，而是通过引流淋巴结中活化B细胞抑制DC所诱导的Th1免疫反应得以实现。

英文摘要：

Ultraviolet irradiation （UV） can induce topical or systemic immunosuppression on skin, but its nature remains unknown. It is hypothesized that in topic immunosuppression, the iC3b-Mo/Mph-mitogenactivated protein kinase （MAPK） signal transduciton pathway induces the phosphorylation of extracellular signal-related kinase p44/42, which in turn causes the production of high levels of IL-10, and accelerates the transformation of mononuclear macrophages to macrophages that could clean out necrotic cells; at the same time, the phosphorylated .p38 MAPK and production of IL-12 were inhibited, which hampers the differentiation and maturation of mononuclear macrophages to CDIc ＋ dendritic cells, and subsequently suppresses T cell-mediated immune response. The UV-induced systemic immunosuppression seems not to be realized by the direct decrease in the number and function of dendritic cells,but via the suppression of dendritic cell-induced Th 1 immune response by activated B cells in draining lymph node.