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. 2021 Jan 21;11:617510. doi: 10.3389/fimmu.2020.617510

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Copyright © 2021 Stenson and Ciorba

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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Activation of TLR2/TLR4 on pericryptal macrophages drives wound healing and radioprotection. Pericryptal macrophages express TLR2 and TLR4. TLR2/TLR4 agonists, including LTA, LPS and HA, drive epithelial proliferation as part of wound healing. Exogenous TLR2/TLR4 agonists, including LTA, LPS, and HA, induce radioprotection by blocking radiation-induced apoptosis. Activation of TLR2 by LTA or activation of TLR4 by LPS or HA results in the release of the chemokine CXCL12, which binds to CXCR4 on COX-2 expressing MSCs. Activation of CXCR4 results in the migration of the MSCs to a site adjacent to the pericryptal macrophages and also adjacent to LGR5+ epithelial stem cells. PGE₂ released by MSCs binds to EP2 on the LGR5+ epithelial stem cells transactivating EGFR, promoting proliferation and blocking radiation-induced apoptosis. Inhibition of CXCR-4 (AMD3100) blocks radioprotection induced by TLR activation.