Résumé
DX 5 + CD 4 + T cells have been shown to dampen collagen‐induced arthritis and delayed‐type hypersensitivity reactions in mice. These cells are also potent modulators of T ‐helper cell responses through direct effects on CD 4 + T cells in an IL ‐4 dependent manner. To further characterize this T ‐cell population, we studied their effect on DC s and the potential consequences on T ‐cell activation. Here, we show that mouse DX 5 + CD 4 + T cells modulate DC s by robustly inhibiting IL ‐12 production. This modulation is IL ‐10 dependent and does not require cell contact. Furthermore, DX 5 + CD 4 + T cells modulate the surface phenotype of LPS ‐matured DC s. DC s modulated by DX 5 + CD 4 + T ‐cell supernatant express high levels of the co‐inhibitor molecules PDL ‐1 and PDL ‐2. OVA ‐specific CD 4 + T cells primed with DC s exposed to DX 5 + CD 4 + T ‐cell supernatant produce less IFN ‐γ than CD 4 + T cells primed by DC s exposed to either medium or DX 5 − CD 4 + T ‐cell supernatant. The addition of IL ‐12 to the co‐culture with DX 5 + DC s restores IFN ‐γ production. When IL ‐10 present in the DX 5 + CD 4 + T ‐cell supernatant is blocked, DC s re‐establish their ability to produce IL ‐12 and to efficiently prime CD 4 + T cells. These data show that DX 5 + CD 4 + T cells can indirectly affect the outcome of the T ‐cell response by inducing DC s that have poor T h1 stimulatory function.