Interleukin 35: protective role and mechanism in type 1 diabetes
Autor: | Si-Ming Zhang, Jun Liang, Ji-Ping Xia, Li Li, Li Zheng, Ya-Lan Wang, Yan-Hong Li, Yan Li, Yu Lu |
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Jazyk: | angličtina |
Rok vydání: | 2023 |
Předmět: | |
Zdroj: | Central European Journal of Immunology, Vol 48, Iss 1, Pp 48-53 (2023) |
Druh dokumentu: | article |
ISSN: | 1426-3912 1644-4124 |
DOI: | 10.5114/ceji.2023.125043 |
Popis: | Interleukin 35 (IL-35), a cytokine secreted by regulatory T (Treg) cells from the differentiation of conventional CD4+ T cells, is a member of the IL-12 family. The IL-12 family of cytokines exhibits an anti-inflammatory property. IL-35 has recently been shown to influence the immune modulation in various diseases, including inflammatory bowel disease, Graves’ disease, rheumatoid arthritis, colitis, psoriasis, and type 1 diabetes (T1D). T1D is an immune-related disease caused by destruction of pancreatic cells, characterized by an absolute lack of insulin. Recently, studies have suggested that protective effects of IL-35 work by improving blood glucose levels and preventing an attack of inflammatory factors on the islets. The protective mechanism may be closely related to the anti-inflammatory properties of IL-35, which include regulating macrophage phenotype, suppressing T cell proliferation, decreasing the differentiation of Th17 cells, increasing the Treg cell population, and inducing IL-35-producing regulatory T cells (iTr35). Here, we review the protective effects and mechanisms of action of IL-35 in T1D. |
Databáze: | Directory of Open Access Journals |
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