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. 2022 Jun 27;13:893365. doi: 10.3389/fimmu.2022.893365

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Copyright © 2022 Radovani and Gudelj

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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Overview of altered N-glycosylation pathways regarding T cells during chronic inflammation. (A) Differentiation of lymphocytes and thus their surface N-glycome is under the direct influence of cytokines and stimulation by antigen presenting cells (APCs). Cytokines control differentiation in favor of proinflammatory T cells (Th1, Th17, Tfh), thereby altering their N-glycome by dysregulating the expression of glycosyltransferases such as MGAT5, ST6GAL1 and FUT8 and abrogating substrate availability for the hexosamine biosynthesis pathway (HBP). The resulting N-glycan changes significantly reduce the binding affinity of inhibitory galectins and Siglecs. (B) Schematic representation of the relevant cytokines responsible for the T cell differentiation. GLUT, glucose transporter; TCR, T cell receptor; Tfh, T follicular helper cell; Th, T helper cell; Treg, T regulatory cell.