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, 88 (2), 227-32

Mycobacterium Tuberculosis Induces IL-17A Responses Through TLR4 and dectin-1 and Is Critically Dependent on Endogenous IL-1

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Mycobacterium Tuberculosis Induces IL-17A Responses Through TLR4 and dectin-1 and Is Critically Dependent on Endogenous IL-1

Frank L van de Veerdonk et al. J Leukoc Biol.

Abstract

In the present study, we dissected the pathways that trigger the IL-17A responses by MTB. Dectin-1 and TLR4 were shown to be involved in MTB-induced IL-17A production, and blockade of the NOD2, TLR2, or MR had no effect on IL-17A. The MAPK Erk, known to mediate transcription of IL-1beta mRNA, was strongly involved in the IL-17A production induced by MTB. The intracellular enzymes caspase-1 and serine proteases, which process pro-IL-1beta into the active IL-1beta, were also crucial for the induction of IL-17A. Lastly, the MTB-induced IL-17A response was strongly dependent on signaling through the IL-1R but not the IL-6R pathway. In conclusion, the MTB-induced IL-17A response relies strongly on the endogenous IL-1 pathway and IL-1R signaling. TLR4 and dectin-1 are the main receptors responsible for mediating the signals responsible for IL-17A production by MTB. These findings contribute to a better understanding of the host response to mycobacteria and provide the opportunity to explore potential, novel, therapeutic strategies against TB.

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