Vγ1+ γδ T cells reduce IL-10-producing CD4+CD25+ T cells in the lung of ovalbumin-sensitized and challenged mice.

In OVA-sensitized and challenged mice, gammadelta T cells expressing Vgamma1 enhance airway hyperresponsiveness (AHR) but the underlying mechanism is unclear. These cells also reduce IL-10 levels in the airways, suggesting that they might function by inhibiting CD4(+)CD25(+) regulatory T cells (T(reg)) or other CD4(+) T cells capable of producing IL-10 and suppressing AHR. Indeed, sensitization and challenge with OVA combined with inactivation of Vgamma1(+) cells increased CD4(+)CD25(+) cells in the lung, and markedly those capable of producing IL-10. The cellular change was associated with increased IL-10 and TGF-beta levels in the airways, and a decrease of IL-13. T(reg) include naturally occurring Foxp3(+) T(reg), inducible Foxp3(-) T(reg), and antigen-specific T(reg) many of which express folate receptor 4 (FR4). Although Foxp3 gene expression in the lung was also increased pulmonary CD4(+) T cells, expressing Foxp3-protein or FR4 remained stable. Therefore, the inhibition by Vgamma1(+) gammadelta T cells might not be targeting Foxp3(+) T(reg) but rather CD4(+) T cells destined to produce IL-10.