TLR and B cell receptor signals to B cells differentially program primary and memory Th1 responses to Salmonella enterica.

Protective Th1 responses to Salmonella enterica do not develop in the absence of B cells. Using chimeric mice, we dissect the early (innate) and late (cognate) contributions of B cells to Th programming. B cell-intrinsic MyD88 signaling is required for primary effector Th1 development, whereas Ag-specific BCR-mediated Ag presentation is necessary for the development of memory Th1 populations. Programming of the primary T cell response is BCR/B cell MHC II independent, but requires MyD88-dependent secretion of cytokines by B cells. Chimeras in which B cells lack IFN-gamma or IL-6 genes make impaired Th1 or Th17 responses to Salmonella.