December 1, 2023

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First discovery of interleukin IL-17D receptor

First discovery of interleukin IL-17D receptor


First discovery of interleukin IL-17D receptor.  The IL-17 family consists of six members (including IL-17A, B, C, D, E, and F). IL-17D is the least understood member of the IL-17 family, and its receptor is not yet clear.

First discovery of interleukin IL-17D receptor


On April 13, 2021, the team of Academician Dong Chen from the School of Medicine of Tsinghua University published an online study titled Interleukin-17D regulates group 3 innate lymphoid cell function through its receptor CD93 (2) on Immunity. The study found that IL-17D derived from intestinal epithelial cells can play a key role in regulating the function of type III intrinsic lymphoid cells (ILC3s) and maintaining intestinal homeostasis by binding to its receptor CD93.

First discovery of interleukin IL-17D receptor


What are the physiological functions of IL-17D?

The researchers first detected the expression of IL-17D in mouse tissues, and found that IL17D is highly expressed in the colon and lungs of mice, suggesting that IL-17D may play important functions in these two organs.

First discovery of interleukin IL-17D receptor

The authors further studied the role of IL-17D in DSS-induced colitis, and found that IL-17D-deficient mice showed more severe enteritis, and administration of exogenous IL-17D to mice could reduce IL-17D-deficient mice The severity of colitis suggests that IL-17D has an important protective effect in colitis.
First discovery of interleukin IL-17D receptor



What cell is IL-17D secreted by?

The source of IL-17D cells was explored by isolating CD45 + and CD45-cells from mouse colon tissue, and it was found that CD45-cells (mainly colonic epithelial cells) highly expressed Il17d mRNA, suggesting that colonic epithelial cells may be IL-17D Main source.


What cell does IL-17D function on?

The results showed that in the colitis model, IL-17D-deficient mice had significantly reduced expression of IL-22, Reg3b and Reg3g, suggesting that IL-17D is a key factor in the production of IL-22 in the intestine.

By constructing the IL-17D-hIg fusion protein, it was found that IL-17D-hIg can specifically bind to ILC3 in the lamina propria lymphocytes of the small intestine, but not T cells, dendritic cells or macrophages. In addition, in IL-17D-deficient mice, the IL-22 expression of ILC3s was significantly reduced. These results indicate that IL-17D plays an important role in maintaining the normal function of intestinal ILC3 cells.

Through RNA-seq analysis, it was found that in IL-17D-deficient ILC3 cells, the expression of some characteristic genes related to ILC1 cells and ILC2 cells was up-regulated, while the expression of characteristic genes in ILC3 cells decreased, suggesting that IL-17D may maintain ILC3-related genes. Expression to regulate the plasticity and stability of ILC3.

In addition, given that IL-22-secreting ILC3s is essential for maintaining intestinal microbial homeostasis, the authors also performed 16S rRNA sequencing analysis on the feces of wild-type and IL17D-deficient mice, and found that IL17D-deficiency led to intestinal microbiota imbalance. And may therefore aggravate the development of colitis.




(source:internet, reference only)

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