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. 2021 May 31;12:670286. doi: 10.3389/fimmu.2021.670286

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Copyright © 2021 Schubert, Rohrbach, Schmitt and Stein-Thoeringer

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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Gut microbial metabolites and microbial ligands can exert far reaching influences on T cells and presumably also CAR-T cells. Whereas tryptophan metabolites can act on T cells through the cytoplasmatic aryl hydrocarbon receptor (AhR), bile acid metabolites induce T cell differentiation and change effector functions through actions on vitamin D receptors (VDR), Farnesoid X receptor (FXR), and also through TGR5, PXR or LXR (no shown in this illustration). Short chain fatty acids act on T cells through G-protein coupled receptors 41, 43 or 109 (GPRs), or regulate immune cell differentiation and function through histone deacetylases (HDACs). Bacterial derived membrane fractions or secreted proteins modulate T cells via Toll-like receptors (TLRs) expressed on activated T cells.