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. 2022 Jul 22;13:952338. doi: 10.3389/fimmu.2022.952338

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Copyright © 2022 Su, Zhang, Yang, Tang, Shen, Liu, Ji, Maurer and Jiao

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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Proposed model of the role of Gal-9 and TIM-3 in the pathogenesis of AD. Gal-9, via TIM-3 expressed by T_H1/T_H17 cells, downregulates their numbers, by inhibiting proliferation and the induction of apoptosis (1). The reduction of T_H1/T_H17 immunity leads to T_H2/T_H22 polarization (2). Increased T_H2/T_H22 immunity and cytokines drive type 2 inflammation and disease activity (3) with higher numbers of eosinophils(4) and B cell class switching to IgE and elevated IgE levels (5). This, in turn, may drive further upregulation of Gal-9 and TIM-3 expression (6). MBP (Major basic protein), ECP (Eosinophil cationic protein), EPO (Eosinophilperoxidase), SCF (Stem cell factor), VEGF-A (Vascular endothelial growth factor-A), NGF (Nerve growth factor).