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. 2021 Mar 29;10(4):747. doi: 10.3390/cells10040747

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© 2021 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Treg license LEC via LTα1β2-LTβR to facilitate other immune cell lymphatic migration. In homeostatic conditions, patrolling nTreg maintain LEC LTβR constitutive activation, and permit both Treg and naïve or memory T cell recirculation to maintain immune surveillance. In inflammation, activated Treg with the highest LTα1β2 expression trigger LTβR signaling on LEC and increase VCAM-1 and CCL21, and decrease the intercellular tight junction protein VE-cadherin (VE-cad). These changes facilitate the TEM of other immune cells such as dendritic cells (DC), macrophages (Mϕ), B cells, and T cells (including activated CD4, CD8). Activation of TLR2 by endogenous ligands such as hyaluronan (HA) intensifies LEC LTβR signaling (Adopted from [51]).