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Staphylococcus aureus  ( S. aureus ) is a human pathogen as well as a frequent colonizer of skin and mucosa. This bacterium potently activates conventional T-cells through superantigens and it is suggested to induce T-cell cytokine-production as well as to promote a regulatory phenotype in T-cells in order to avoid clearance. This study aimed to investigate how  S. aureus  impacts the production of regulatory and pro-inflammatory cytokines and the expression of CD161 and HELIOS by peripheral CD4 + FOXP3 +  T-cells. Stimulation of PBMC with  S. aureus  161:2-cell free supernatant (CFS) induced expression of IL-10, IFN-γ and IL-17A in FOXP3 +  cells. Further, CD161 and HELIOS separated the FOXP3 +  cells into four distinct populations regarding cytokine-expression. Monocyte-depletion decreased  S. aureus  161:2-induced activation of FOXP3 +  cells while pre-stimulation of purified monocytes with  S. aureus  161:2-CFS and subsequent co-culture with autologous monocyte-depleted PBMC was sufficient to mediate activation of FOXP3 +  cells. Together, these data show that  S. aureus  potently induces FOXP3 +  cells and promotes a diverse phenotype with expression of regulatory and pro-inflammatory cytokines connected to increased CD161-expression. This could indicate potent regulation or a contribution of FOXP3 +  cells to inflammation and repression of immune-suppression upon encounter with  S. aureus .

Staphylococcus aureus-derived factors induce IL-10, IFN-γ and IL-17A-expressing FOXP3+CD161+ T-helper cells in a partly monocyte-dependent manner