Zusammenfassung
The NF-kappa 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-gamma (IFN-gamma), production by gamma delta T cells required the NF-kappa B family members RelA and ReIB as well as the lymphotoxin-beta-receptor (LT beta R). In contrast, LT beta R-NF-kappa ...
Zusammenfassung
The NF-kappa 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-gamma (IFN-gamma), production by gamma delta T cells required the NF-kappa B family members RelA and ReIB as well as the lymphotoxin-beta-receptor (LT beta R). In contrast, LT beta R-NF-kappa B signaling was not involved in the differentiation of conventional alpha beta Th17 cells. Impaired IL-17 production in ReIA- or ReIB-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 ReIB, acting downstream of LT beta R, was required for the expression of ROR gamma t and ROR alpha 4 transcription factors and the differentiation of thymic precursors into gamma delta T17 cells. Thus, RelA and ReIB within different thymocyte subpopulations cooperate in the regulation of IL-17 production by gamma delta T cells and contribute to the host's ability to fight bacterial infections.
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