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白细胞介素27(IL-27)是一种IL-6/IL-12家族细胞因子,主要由激活的抗原提呈细胞产生,通过激活Janus激酶-信号转导子与转录激活子(JAK-STAT)和丝裂原激活蛋白激酶(MAPK)等信号通路发挥作用。最初认为IL-27能够促进1型辅助T(Th1)细胞、1型调节性T(Tr1)细胞的分化,抑制Th2细胞、Th17细胞、调节性T细胞(Treg)的分化,现在发现对某些T细胞亚群具有相反的效应,比如Treg。IL-27在不同的自身免疫性疾病中表现出促炎和抗炎的双重作用。作为最强大的抗原提呈细胞,树突状细胞(DC)和单核巨噬细胞是适应性免疫的启动者,引起免疫应答或耐受。IL-27对DC和单核巨噬细胞的作用并不一致,而这种差异很可能是由不同信号通路的比率、细胞因子微环境、疾病的发展阶段引起的。阐明IL-27对DC和单核巨噬细胞的影响或许可以及早地阻断异常免疫反应,对自身免疫性疾病的治疗提供新的途径。
Interleukin 27 (IL-27), an IL-6 / IL-12 family of cytokines, is produced primarily by activated antigen-presenting cells by activating Janus kinase-signal transducers and activators of transcription (JAK-STAT ) And mitogen-activated protein kinase (MAPK) and other signaling pathways play a role. IL-27 was initially thought to promote the differentiation of type 1 helper T (Th1) cells and type 1 regulatory T (Tr1) cells and to inhibit the differentiation of Th2 cells, Th17 cells and regulatory T cells (Tregs) T-cell subsets have the opposite effect, such as Treg. IL-27 exhibits a dual role of proinflammatory and anti-inflammatory in different autoimmune diseases. As the most powerful antigen-presenting cells, dendritic cells (DCs) and monocytes are the initiators of adaptive immunity that elicit an immune response or tolerance. The role of IL-27 on DC and monocyte-macrophage cells is not consistent, and this difference is likely to be caused by the ratio of different signaling pathways, the cytokine microenvironment, and the stage of disease progression. To clarify the effect of IL-27 on DC and monocyte-macrophage cells may be able to block the abnormal immune response as early as possible and provide a new approach for the treatment of autoimmune diseases.