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. 2021 Apr 12;12:660203. doi: 10.3389/fimmu.2021.660203

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Copyright © 2021 Lowy, Makker and Moalem-Taylor

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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Reported and speculative neuroimmune interactions within the skin in CIPN and DPN. In a CIPN mouse model, Angiotensin II administration resulted in macrophage release of reactive oxygen species via AT2R. TRPA1 stimulation caused nociceptor excitation. Increased number of activated Langerhans cells may release pro-inflammatory mediators which can sensitize nociceptors. Altered expression of neurotrophins such as NT-3 may affect immune and neuronal function; elevated levels of mast cell-derived NT-3 associated with reduced IL-8 production from keratinocytes in skin of AD patients. In DPN, abnormal neurotrophin signalling may disrupt keratinocyte and neuronal function. Bradykinin administration was shown to upregulate inflammatory neuropeptides SP and CGRP and inflammatory lipid PGE2. Further, increased macrophage infiltration was observed in the skin of diabetic mice.