Copyright
©The Author(s) 2018.
World J Diabetes. Dec 15, 2018; 9(12): 220-225
Published online Dec 15, 2018. doi: 10.4239/wjd.v9.i12.220
Published online Dec 15, 2018. doi: 10.4239/wjd.v9.i12.220
Figure 1 Innate-like T cells employ syndecan-1 to regulate interleukin-17 production.
Homeostasis of interleukin (IL)-17 production by natural killer T (NKT) and γδ T cells in wild type (left) and syndecan-1-deficient (right) mice. The diagram illustrated significant increases in numbers of NKT17 and Tγδ17 subsets in the thymus and in peripheral organs thereby increasing genetic susceptibility to IL-17-driven autoimmune diseases. IL-17: Interleukin-17; NKT: Natural killer T cells; Sdc1: Syndecan-1; KO: Knockout; NKT17: Interleukin-17-producing subsets of natural killer T cells; Tγδ17: Interleukin-17-producing subsets of γδ T cells; iNKT: Invariant natural killer T cells.
- Citation: Jaiswal AK, Sadasivam M, Hamad ARA. Unexpected alliance between syndecan-1 and innate-like T cells to protect host from autoimmune effects of interleukin-17. World J Diabetes 2018; 9(12): 220-225
- URL: https://www.wjgnet.com/1948-9358/full/v9/i12/220.htm
- DOI: https://dx.doi.org/10.4239/wjd.v9.i12.220