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Aim: Tyro3,Axl and Mer constitute the TAM family of receptor tyrosine kinases (RTKs) characterized by a conserved sequence within the kinase domain and adhesion molecule-like extracellular domains.Absence of TAM receptors are easily to happen autoimmunity-like diseases that contribute to both sustained APC hyperactivation and the delayed phagocytic clearance of apoptotic cells.Methods: In this work,we frist identify that the expressions of Axl and Mer receptor mRNA and protein were shown on BALB/c mice CD4+CD25+Tregs.Apart from this,we also found that Gas6 enhances suppressive capacity of Tregs.Gas6-induced effect might depend on up-regualtion of Foxp3 as well as CTLA-4 expression,and,promote the immunosupressive cytokines of IL-1O,TGF-β1 produce.Meanwhile,IL-2,the ratio of IFN-γ/IL-4 in CD4+CD25+Treg/CD4+CD25- T cell coculture supernatant were determined to examine the effects of Gas6 0n the T-cell proliferation and differentiation induced by CD4+CD25+Tregs.Results: We observed that a decrease in the concentration of IL-2 in Gas6-stimulated groups,and,the ratio of IFN-γ/IL-4 were also decrease.To identify which receptor play the dominant role,we used the antagonist of the Axl and Mer receptors to block these receptors activated.Our datas demonstrated that blocking the Axl receptor can significantly reversed the Gas6-induced Tregs effect,but blocking the Mer receptor we did not observed the influence of the Gas6-induced Tregs effect.Conclusion: Axl receptor seems to be a new critical regulator for immunosuppressive function of CD4+CD25+Tregs.