Immune requirements for protective Th17 recall responses to Mycobacterium tuberculosis challenge.

摘要: Tuberculosis (TB) vaccine development has focused largely on targeting T helper type 1 (Th1) cells. However, despite inducing Th1 cells, the recombinant TB MVA85A failed to enhance protection against disease in humans. In recent years, Th17 cells have emerged as key players vaccine-induced TB. exact cytokine and immune requirements that enable Th17-induced recall remain unclear. this study, we investigated for cell-induced Mycobacterium tuberculosis (Mtb) challenge by utilizing a tractable adoptive transfer model mice. We demonstrate of Mtb-specific into naive hosts, upon Mtb challenge, results responses confer at levels similar vaccination strategies. Importantly, although interleukin (IL)-23 is critical, IL-12 IL-21 are dispensable protective responses. Unexpectedly, interferon-γ (IFN-γ) produced adoptively transferred impairs long-lasting immunity challenge. contrast, CXCR5 expression crucial localization near macrophages within well-formed B-cell follicles mediate control. Thus, our data identify new characteristics can be harnessed improve enhancing design