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Regulatory CD8 +  T cells are critical for self-tolerance and restricting excessive immune responses. The variety of immune functions they fulfill, the heterogeneity of their phenotype, and the mechanism of action are still poorly understood. Here we describe that regulatory CD8 +  T cells exhibiting immunosuppressive actions  in vitro  and  in vivo  are recognized as CD38 high  T cells and present in naive mice. CD38 is a glycosylated membrane protein with ectonucleotidase properties. CD8 + CD38 high  (CD44 + CD122 + CD62L high ) lymphocytes suppress CD4 +  effector T-cell proliferation in an antigen-non specific manner via IFN-γ. While direct cell-to-cell contact is needed for this suppressor activity, it is independent of membrane-bound TGF-β and granzyme B release. IL-15 potentiates the suppressive activity of CD8 + CD38 high  T cells and controls their survival and expansion. In humans CD8 + CD38 high  T cells inhibit CD4 +  effector T cell proliferation.  In vivo , CD8 + CD38 high , but not CD8 + CD38 −  T cells mitigate murine experimental autoimmune encephalomyelitis (EAE) by reducing the clinical score and delaying disease occurrence. EAE suppression is enhanced by pre-treatment of CD8 + CD38 high  T cells with IL-15. These findings add evidence that the expression of ectoenzyme receptor family members positively correlates with suppressor functions and identifies CD8 + CD38 high  T cells as potential inhibitors of excessive immune responses.

Ectonucleotidase CD38 Demarcates Regulatory, Memory-Like CD8+ T Cells with IFN-γ-Mediated Suppressor Activities