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免疫调节细胞因子白细胞介素-35与免疫性血小板减少症

Immunomodulatory cytokine interleukin-35 and immune thrombocytopaenia.

作者信息

Zhu Jing-Jing, Shan Ning-Ning

机构信息

Department of Haematology, 34708Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong Province, China.

出版信息

J Int Med Res. 2020 Dec;48(12):300060520976477. doi: 10.1177/0300060520976477.

DOI:10.1177/0300060520976477
PMID:33356722
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7768574/
Abstract

Considerable attention has been paid to interleukin (IL)-35 because of its immunosuppressive effects in a variety of autoimmune diseases. IL-35, a recently identified cytokine of the IL-12 family, is a negative regulatory factor secreted by IL-35-inducible regulatory T cells (iTr35 cells) and the recently reported regulatory B cells (B cells). Four biological effects of IL-35 have been discovered and : (i) suppression of T cell proliferation; (ii) conversion of naive T cells into iTr35 cells; (iii) downregulation of type 17 helper T (T17) cells; and (iv) conversion of B cells into a B subset that produces IL-35 and IL-10. IL-35 plays an important role in a variety of autoimmune diseases, such as rheumatoid arthritis, allergic asthma and systemic lupus erythematosus. Primary immune thrombocytopaenia (ITP), which is characterized by isolated thrombocytopaenia and mild mucocutaneous to life-threatening bleeding, is an autoimmune disease with complex dysregulation of the immune system. Both antibody-mediated and/or T cell-mediated platelet destruction are key processes. In addition, impairment of T cells and cytokine imbalances have now been recognized to be important. This review summarizes the immunomodulatory effects of IL-35 and its role in the pathogenesis of ITP as mediated by T and B cells.

摘要

由于白细胞介素(IL)-35在多种自身免疫性疾病中具有免疫抑制作用,因此受到了广泛关注。IL-35是IL-12家族中最近发现的一种细胞因子,是由IL-35诱导性调节性T细胞(iTr35细胞)和最近报道的调节性B细胞(B细胞)分泌的负调节因子。已经发现IL-35有四种生物学效应:(i)抑制T细胞增殖;(ii)将初始T细胞转化为iTr35细胞;(iii)下调17型辅助性T(T17)细胞;(iv)将B细胞转化为产生IL-35和IL-10的B细胞亚群。IL-35在多种自身免疫性疾病中起重要作用,如类风湿性关节炎、过敏性哮喘和系统性红斑狼疮。原发性免疫性血小板减少症(ITP)以孤立性血小板减少和轻度黏膜皮肤出血至危及生命的出血为特征,是一种免疫系统复杂失调的自身免疫性疾病。抗体介导和/或T细胞介导的血小板破坏都是关键过程。此外,现在已经认识到T细胞功能障碍和细胞因子失衡很重要。本综述总结了IL-35的免疫调节作用及其在T和B细胞介导的ITP发病机制中的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5df1/7768574/8a411381cda3/10.1177_0300060520976477-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5df1/7768574/bb926ea559a2/10.1177_0300060520976477-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5df1/7768574/aad1026cd58e/10.1177_0300060520976477-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5df1/7768574/8a411381cda3/10.1177_0300060520976477-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5df1/7768574/bb926ea559a2/10.1177_0300060520976477-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5df1/7768574/aad1026cd58e/10.1177_0300060520976477-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5df1/7768574/8a411381cda3/10.1177_0300060520976477-fig3.jpg

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JAK/STAT signaling is involved in IL-35-induced inhibition of hepatitis B virus antigen-specific cytotoxic T cell exhaustion in chronic hepatitis B.JAK/STAT 信号通路参与了白细胞介素-35 诱导的慢性乙型肝炎中乙型肝炎病毒抗原特异性细胞毒性 T 细胞耗竭的抑制作用。
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