Center for Neuroimmunology & Neuroinfectious Diseases, Washington University School of Medicine, St. Louis, MO, United States.
Department of Medicine, Washington University School of Medicine, St. Louis, MO, United States.
Front Immunol. 2021 Nov 26;12:764062. doi: 10.3389/fimmu.2021.764062. eCollection 2021.
Type III interferons (IFNs) or the lambda IFNs (IFNLs or IFN-λs) are antimicrobial cytokines that play key roles in immune host defense at endothelial and epithelial barriers. IFNLs signal their heterodimeric receptor, comprised of two subunits, IFNLR1 and interleukin (IL)10Rβ, which defines the cellular specificity of the responses to the cytokines. Recent studies show that IFNL signaling regulates CD4+ T cell differentiation, favoring Th1 cells, which has led to the identification of IFNL as a putative therapeutic target for autoimmune diseases. Here, we summarize the IFNL signaling pathways during antimicrobial immunity, IFNL-mediated immunomodulation of both innate and adaptive immune cells, and induction of autoimmunity.
III 型干扰素（IFNs）或 lambda 干扰素（IFNLs 或 IFN-λs）是抗菌细胞因子，在血管内皮和上皮屏障的宿主免疫防御中发挥关键作用。IFNLs 通过其异二聚体受体发出信号，该受体由两个亚基 IFNLR1 和白细胞介素（IL）10Rβ 组成，这决定了细胞对细胞因子反应的特异性。最近的研究表明，IFNL 信号转导调节 CD4+T 细胞分化，有利于 Th1 细胞，这导致了 IFNL 作为自身免疫性疾病的潜在治疗靶点的鉴定。在这里，我们总结了抗菌免疫过程中的 IFNL 信号通路、IFNL 对先天和适应性免疫细胞的免疫调节以及自身免疫的诱导。
