Allergic Airway Hyperresponsiveness-Enhancing γδ T Cells Develop in Normal Untreated Mice and Fail to Produce IL-4/13, Unlike Th2 and NKT Cells

摘要: Allergic airway hyperresponsiveness (AHR) in OVA-sensitized and challenged mice, mediated by allergen-specific Th2 cells Th2-like invariant NKT (iNKT) cells, develops under the influence of enhancing inhibitory γδ T cells. The AHR-enhancing belong to Vγ1+ cell subset, that are capable increasing IL-5 IL-13 levels airways a manner like They also synergize with iNKT mediating AHR. However, unlike AHR enhancers arise untreated we show here they exhibit their functional bias already as thymocytes, at an HSAhigh maturational stage. In further contrast could not be stimulated produce IL-4 IL-13, consistent synergistic dependence on Mice deficient IFN-γ, TNFRp75, or did these but absence spontaneous development was restored adoptive transfer IFN-γ-competent dendritic from donors. i.p. injection OVA/aluminum hydroxide all mutant strains, indicating still can induced when fail develop spontaneously, themselves need express exert function. We conclude both cytokine potential differs critically despite similar influences populations