Mucosa-associated invariant T (MAIT) cells are a subpopulation of unconventional T cells that exert potent antibacterial responses when activated in an MHC class Ib protein (MR1)-dependent manner. The production of effector cytokines such as interferon gamma (IFNγ), tumour necrosis factor (TNF) and cytolytic proteins such as granzyme B (GrzB), induce effective lysis and elimination of infected cells. Conversely, maintenance of self-tolerance and response towards excessive inflammation are mediated by regulatory T cells (Treg) that express high levels of the IL-2 receptor-α subunit CD25. Treg cells dampen the effector responses and suppress proliferation of effector T cell populations through various mechanism, including the release of immunosuppressive cytokines, such as IL-10. The properties of Treg cells have garnered interest as a therapeutic target, however their modulations on MAIT cells have yet to be elucidated
Here, we report development of a novel assay to examine the mechanisms of Treg cell immunosuppression on MAIT cell activation. Treg cells and CD25neg effector T cell populations were either depleted from, or isolated and expanded from, peripheral blood mononuclear cells (PBMCs). Following activation with Escherichia coli, the MAIT cell population in Treg cell-depleted PBMCs had increased TNF production compared to those in total PBMCs. MAIT cells cocultured with supernatant from anti-CD3/CD28 bead-activated Treg cell cultures exhibited a decreased functional response with lower expression of GrzB, CD107a, and TNF, compared to MAIT cells cocultured with CD25neg effector T cell supernatant. Compared to CD25neg T effector cells, Treg cell culture supernatant had increased levels of IL-10, IL-4, and IL-13 cytokines that was sustained up to 72 hours after activation.
These data are the first step in uncovering the interplays between these two specialized T cell subsets and identifying novel approaches to modulate excessive MAIT cell function in the setting of intestinal chronic inflammatory diseases such as inflammatory bowel disease.