CAJ | 학술논문

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CDlc+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.
국부면역억제경iC3b-Mo/Mph-사렬원활화단백격매신호전도도경,유도세포외신호조절격매p44/42린산화,산생고수평적IL-10,촉진단핵거서세포조거서세포적방향발전,이탄서UV폭로부위적배사세포.동시억제린산화p38사렬원활화단백격매화IL-12적산생,조애단핵거서세포향CDlc+수돌세포방향분화화성숙,이억제T세포주도적면역반응.재UV인기적계통성면역억제중,기궤제병비통과직접억제DC적수량화공능,이시통과인류림파결중활화B세포억제DC소유도적Th1면역반응득이실현.
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-mitogen-activated protein kinase (MAPK) signal transduciton pathway induces the phosphorylation of extracellular signal-related kinase 1044/42, 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-modiated 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 Thl immune response by activated B cells in draining lymph node.