CXCR3 and bacterial infectious disease: On the one hand, there is now solid evidence for the idea that Th1-polarized settings of viral or bacterial infection promote Tregs that, like their effector T-cell counterparts, express Tbet and CXCR3 [47]; indeed, we find that H. pylori induces concomitant Th1 and Tbet+ pTreg responses, and that both depend on BATF3.