Abstract
BackgroundDok-3 has been shown to play an important role in immune system. Tim-3 also has been recognized as an important immune regulator which involves in many diseases. The relationship of them is still unclear.MethodsWe detected the expression of Tim-3 on spleen immune cells from Dok-3 deficient mice and control mice by flow cytometry.ResultsIn this article, we found that Dok-3−/− mice display almost entirely different immune clustering characteristics compared with wild type 129 mice. The CD4 T cells and CD8 T cells decreased and DC cells, macrophages, MDSCs increased when the Dok-3 gene knocked-out. The Tim-3 expression on CD4 T cells, CD8 T cells, NK cells, DC cells increased when the Dok-3 gene knocked-out. The macrophages and MDSCs just display the opposite results.ConclusionsAlthough Dok-3−/− mice display different immune clustering and Tim-3 expression, the mechanism still needs further study.
Highlights
downstream of kinase 3 (Dok-3) has been shown to play an important role in immune system
Dok‐3 deficient mice display different immune cell proportions compared with 129 mice We analyzed the CD4 T cells, CD8 T cells, natural killer (NK) cells, dendritic cell (DC) cells, macrophages, myeloid-derived suppressor cell (MDSC) in the spleens from the two mice group
The results show that Dok-3−/− mice have much more MDSCs than 129 mice (129, 9.72 ± 1.886; Dok-3−/−, 23.73 ± 3.150)
Summary
Dok-3 has been shown to play an important role in immune system. Tim-3 has been recognized as an important immune regulator which involves in many diseases. Dok proteins function mainly as adaptors to facilitate protein–protein interactions since they have no catalytic activity [1]. Given Dok-1 to Dok-3 are expressed in the immune cells, they play an important role in the development of the tumor progression. Dok-3 has been shown to play an important role in immune system. It can inhibit the C a2+ [5] and JNK [6] activation in B cell receptor signaling. Dok-3 plays a critical and positive role in TLR3 signaling by enabling TRAF3/TBK1 complex formation and facilitating TBK1 and IFN regulatory factor 3 activation and the induction of IFN-β production [8]
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