The Journal of Immunology · 2010 · 133 citations · 56 references
Immune ActivationMicrobial PathogensAdaptive Immune SystemInnate Immune SystemImmunologyHumoral ResponseCd4 T Cell ResponsesInnate ImmunityImmune SystemCell SignalingImmunological MemoryB CellsTh ProgrammingT Cell ImmunityHumoral ImmunityCell BiologyAdaptive ImmunityProtective Th1 ResponsesImmune Cell DevelopmentPathogenesisMemory Th1 ResponsesCellular Immune ResponseMedicineImmune Cell Activation
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.
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