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. 2019 Jan 14;9:3170. doi: 10.3389/fimmu.2018.03170

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Copyright © 2019 Beringer, Gouriou, Lavocat, Ovize and Miossec.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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IL-17 and TNFα mediate muscle damage and weakness through immune and non-immune pathways in myoblasts. The immune cell infiltration in IIM constitutes a local source of cytokines and promotes the cell-cell interactions. IL-17 mainly produced by Th17 cells, and TNFα act in synergy on myoblasts to increase IL-6 and CCL20 secretion. Because IL-6 is involved in the Th17 cell differentiation and CCL20 in dendritic and Th17 cell recruitment, IL-6 and CCL20 mediate a positive feedback loop promoting local IL-17 production. IL-17 and TNFα induce also non-immune pathways with ROS production, ER stress and SOCE activation. The IL-17/TNFα effect of mitochondrial dysfunction, ER stress, and SOCE activation are probably closely linked. SOCE and calcium dysregulation contribute to the IL-6 release induced by IL-17/TNFα. CCL20, chemokine (C-C motif) ligand 20; DC, dendritic cells; ER, endoplasmic reticulum; IL, interleukin; ROS, reactive oxygen species; STIM, stromal interacting molecule; TNFα, tumor necrosis factor-α.