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Publication : Gut-associated lymphoid tissue attrition associates with response to anti-α4β7 therapy in ulcerative colitis.

First Author	Canales-Herrerias P	Year	2024
Journal	Sci Immunol	Volume	9
Issue	94	Pages	eadg7549
PubMed ID	38640252	Mgi Jnum	J:358612
Mgi Id	MGI:7782806	Doi	10.1126/sciimmunol.adg7549
Citation	Canales-Herrerias P, et al. (2024) Gut-associated lymphoid tissue attrition associates with response to anti-alpha4beta7 therapy in ulcerative colitis. Sci Immunol 9(94):eadg7549

abstractText

Vedolizumab (VDZ) is a first-line treatment in ulcerative colitis (UC) that targets the alpha4beta7- mucosal vascular addressin cell adhesion molecule 1 (MAdCAM-1) axis. To determine the mechanisms of action of VDZ, we examined five distinct cohorts of patients with UC. A decrease in naive B and T cells in the intestines and gut-homing (beta7(+)) plasmablasts in circulation of VDZ-treated patients suggested that VDZ targets gut-associated lymphoid tissue (GALT). Anti-alpha4beta7 blockade in wild-type and photoconvertible (KikGR) mice confirmed a loss of GALT size and cellularity because of impaired cellular entry. In VDZ-treated patients with UC, treatment responders demonstrated reduced intestinal lymphoid aggregate size and follicle organization and a reduction of beta7(+)IgG(+) plasmablasts in circulation, as well as IgG(+) plasma cells and FcgammaR-dependent signaling in the intestine. GALT targeting represents a previously unappreciated mechanism of action of alpha4beta7-targeted therapies, with major implications for this therapeutic paradigm in UC.

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