IL-23 is required for the IL-17 response to infection with Mycobacterium tuberculosis (Mtb), but is not required for the early control of bacterial growth. However, mice deficient for the p19 component of IL-23 (Il23a−/−) exhibit increased bacterial growth late in infection that is temporally associated with smaller B cell follicles in the lungs. Cxcl13 is required for B cell follicle formation and immunity during tuberculosis. The absence of IL-23 results in decreased expression of Cxcl13 within Mtb-induced lymphocyte follicles in the lungs and this deficiency was associated with increased cuffing of T cells around the vessels in the lungs of these mice. Il23a−/− mice also poorly expressed IL-17A and IL-22 mRNA. These cytokines were able to induce Cxcl13 in mouse primary lung fibroblasts suggesting that these cytokines are likely involved in B cell follicle formation. Indeed, IL-17RA-deficient mice (Il17ra−/−) generated smaller B cell follicles early in the response, whereas IL-22-deficient (Il22−/−) mice had smaller B cell follicles at an intermediate time after infection; however only Il23a−/− mice had a sustained deficiency in B cell follicle formation and reduced immunity. We propose that in the absence of IL-23, expression of long-term immunity to tuberculosis is compromised due to reduced expression of Cxcl13 in B cell follicles and reduced ability of T cells to migrate from the vessels and into the lesion. Further while IL-17 and IL-22 can both contribute to Cxcl13 production and B cell follicle formation it is IL-23 that is critical in this regard.