Figure 1 New therapeutic approaches in IBD therapy based on blockade of T-cell homing and retention Figure 1 | New therapeutic approaches in IBD therapy.

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Figure 1 New therapeutic approaches in IBD therapy based on blockade of T-cell homing and retention Figure 1 | New therapeutic approaches in IBD therapy based on blockade of T-cell homing and retention. Several new drugs — vedolizumab, anti-MAdCAM1 antibodies and etrolizumab — target T-cell homing and retention as a therapeutic target in IBD. Specifically, inhibition of the interaction between α4β7 integrins on T cells with MAdCAM1 on gut endothelial cells (via vedolizumab or etrolizumab) blocks homing of TH1, TH2, TH17 and Treg cells to the inflamed colon in IBD and their subsequent accumulation in the tissue. Moreover, targeting of the interaction between αE on intestinal T cells with E-cadherin on gut epithelial cells (via etrolizumab) inhibits the retention of TH9 and CD8+ T cells in the inflamed tissue in IBD. Thus, targeting of both T-cell homing and retention affects T-cell trafficking and might be used to suppress local T-cell accumulation in gut inflammation. MAdCAM1, mucosal addressin cell adhesion molecular 1; TH1, type 1 T helper cell; TH2, type 2 T helper cell; TH9, type 9 T helper cell; TH17, type 17 T helper cell; Treg, regulatory T cell; VCAM1, vascular adhesion protein 1. Neurath, M. F. (2016) Current and emerging therapeutic targets for IBD Nat. Rev. Gastroenterol. Hepatol. doi:10.1038/nrgastro.2016.208