The NF-?B transcription factor regulates numerous immune responses but its contribution to interleukin-17 (IL-17) production by T cells is largely unknown. Here, we report that IL-17, but not interferon-? (IFN-?), production by ?? T cells required the NF-?B family members RelA and RelB as well as the lymphotoxin-?-receptor (LT?R). In contrast, LT?R-NF-?B signaling was not involved in the differentiation of conventional ?? Th17 cells. Impaired IL-17 production in RelA- or RelB-deficient T cells resulted in a diminished innate immune response to Escherichia coli infection. RelA controlled the expression of LT ligands in accessory thymocytes whereas RelB, acting downstream of LT?R, was required for the expression of ROR?t and ROR?4 transcription factors and the differentiation of thymic precursors into ??T17 cells. Thus, RelA and RelB within different thymocyte subpopulations cooperate in the regulation of IL-17 production by ?? T cells and contribute to the host's ability to fight bacterial infections.     «

The NF-?B transcription factor regulates numerous immune responses but its contribution to interleukin-17 (IL-17) production by T cells is largely unknown. Here, we report that IL-17, but not interferon-? (IFN-?), production by ?? T cells required the NF-?B family members RelA and RelB as well as the lymphotoxin-?-receptor (LT?R). In contrast, LT?R-NF-?B signaling was not involved in the differentiation of conventional ?? Th17 cells. Impaired IL-17 production in RelA- or RelB-deficient T cells r...     »