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The role of IL-10 in immune regulation




The IL-10 family of cytokines consists of nine members: IL-10, IL-19, IL-20, IL-22, IL-24, IL-26, IL-28A, IL-28B, and IL-29. IL-10 family cytokines emerged before the adaptive immune response. IL-10 family cytokines are essential for maintaining the integrity and homeostasis of tissue epithelial layers. Members of this family can promote innate immune responses from tissue epithelia to limit the damage caused by viral and bacterial infections. These cytokines can also facilitate the tissue-healing process in injuries caused by infection or inflammation. 


IL-10 can repress proinflammatory responses and limit unnecessary tissue disruptions caused by inflammation. More than 20 years ago, IL-10 was identified as a “cytokine synthesis inhibitory factor,” a product of Th2 clones following protein or antigen stimulation, that blocked cytokine production from Th1 clones. IL-10 achieved this effect by inhibiting the ability of myeloid cells such as macrophages and dendritic cells (DCs) to activate Th1 cells. 

ELISA(enzyme-linked immunosorbent assay) is a method for detecting the concentration of some kind antigen or antibody,such as IL-10, using the characteristic of specific binding between antigen-antibody. Meretciel provide high quality ELISA kits for R&D,can study the role of IL-10 in immune regulation.


We now know that IL-10 is not just made by Th2 cells, but can be produced by most CD4+ T-cell subsets, including Th1 and Th17 cells, B cells, neutrophils, macrophages, and some DC subsets. Regulatory T cells (Tregs) also serve as a major source of immunoregulatory IL-10. IL-10 depending on their developmental origin, may come in several forms. 


Thymic and inducible Tregs expressing the transcription factor FoxP3+(FoxP3+ Treg) can suppress effector responses through the soluble factors transforming growth factor-β (TGF-β) and IL-10, as well as via cell–cell contact mechanisms such as cytotoxic T-lymphocyte antigen 4 (CTLA-4). FoxP3+ Tregs have been shown during Mtb infection to limit host T-cell accumulation in the lungs and restrict subsequent effector responses; however, it is not clear whether they achieve these effects via the action of IL-10.


 IL-10 signals through a receptor complex consisting of two subunits:IL10R1 and IL10R2. IL10R1 is induced on stimulated hematopoietic cells.And IL10R2 is constitutively expressed on most cells and tissues.These receptor subunits transduce signals through the Janus kinase (Jak)–STAT pathway via Jak1 in the mouse and Jak1 and tyrosine kinase 2 (Tyk2) in humans, culminating in tyrosine phosphorylation and activation of STAT3, as well as STAT1, and in nonmacrophage cells, STAT5. However, the genetic and biochemical evidence from both mouse and human systems implicates STAT3 as the sole STAT required to generate the IL-10 inhibitory signal.



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