A chronic autoimmune condition known as type 1 diabetes mellitus (T1DM) has characteristics marked by a gradual immune-mediated deterioration of the β-cells that produce insulin and causes overt hyperglycemia. it affects more than 1.2 million kids and teenagers (0-19 years old). In both, the initiation and elimination phases of T1DM, cytokine-mediated immunity is crucial in controlling inflammation. T regulatory (Treg) cells, a crucial anti-inflammatory CD4+ T cell subset, secretes interleukin-35 (IL-35). The IL-35 has immunomodulatory properties by inhibiting pro-inflammatory cells and cytokines, increasing the secretion of interleukin-10 (IL-10) as well as transforming Growth Factor- β (TGF-β), along with stimulating the Treg and B regulatory (Breg) cells. IL-35, it is a possible target for cutting-edge therapies for cancers, inflammatory, infectious, and autoimmune diseases, including TIDM. Unanswered questions surround IL-35's function in T1DM. Increasing data suggests Treg cells play a crucial role in avoiding autoimmune T1DM. Throughout this review, we will explain the biological impacts of IL-35 and highlight the most recently progresses in the roles of IL-35 in treatment of T1DM; the knowledge gathered from these findings might lead to the development of new T1DM treatments. This review demonstrates the potential of IL-35 as an effective autoimmune diabetes inhibitor and points to its potential therapeutic value in T1DM clinical trials.
Keywords: IL-35; Possible mechanisms; T1DM; Therapeutic role of IL-35; Treg cells.
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