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Although loss of immune tolerance to bacterial antigens is the likely trigger of the dysregulated immune response that characterizes inflammatory bowel disease (IBD), little effort has been placed on understanding the interface between B cells, IgA, and the microbiota during initiation or progression of disease. This may be in part due to the misleading fact that IgA-deficient humans are mostly asymptomatic, likely due to redundant role of secretory (S) IgM. Intestinal B cell recruitment is critically dependent on integrin \u03b14\u03b27-MAdCAM-1 interactions, yet antibodies that target \u03b14\u03b27 (ie, vedolizumab), MAdCAM-1 (ie, ontamalimab), or both \u03b27 integrins (\u03b14\u03b27 and \u03b1E [CD103] \u03b27; etrolizumab) are in clinical use or development as IBD therapeutics. The effect of such interventions on the biology of IgA is largely unknown, yet a single dose of vedolizumab lowers SIgA levels in stool and weakens the oral immunization response to cholera vaccine in healthy volunteers. Thus, it is critical to further understand the role of these integrins for the migration of ASC and other cellular subsets during homeostasis and IBD-associated inflammation and the mode of action of drugs that interfere with this traffic. We have recently identified a subset of mature ASC that employs integrin \u03b1E\u03b27 to dock with intestinal epithelial cells, predominantly in the pericryptal region of the terminal ileum. This role for the integrin had not been appreciated previously, nor the \u03b1E\u03b27-dependent mechanism of IgA transcytosis that it supports. Furthermore, we find that B cells more than T cells are critically dependent on \u03b14\u03b27-MAdCAM-1 interactions; thus MAdCAM-1 blockade and integrin-\u03b27 deficiency counterintuitively hasten colitis in interleukin-10-deficient mice. In both cases, de novo recruitment of IgA ASC to the intestinal lamina propria is compromised, leading to bacterial overgrowth, dysbiosis, and lethal colitis. Thus, despite the safe and effective use of anti-integrin antibodies in patients with IBD, much remains to be learned about their various cell targets.<\/jats:p>","DOI":"10.1093\/ibd\/izad024","type":"journal-article","created":{"date-parts":[[2023,3,22]],"date-time":"2023-03-22T01:58:58Z","timestamp":1679450338000},"page":"1327-1341","source":"Crossref","is-referenced-by-count":35,"title":["The Underappreciated Role of Secretory IgA in IBD"],"prefix":"10.1093","volume":"29","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5492-5717","authenticated-orcid":false,"given":"Giorgos","family":"Bamias","sequence":"first","affiliation":[{"name":"GI Unit, 3rd Academic Department of Internal Medicine, National and Kapodistrian University of Athens, Sotiria Hospital , Athens , Greece"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Konstantina","family":"Kitsou","sequence":"additional","affiliation":[{"name":"GI Unit, 3rd Academic Department of Internal Medicine, National and Kapodistrian University of Athens, Sotiria Hospital , Athens , Greece"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7887-7959","authenticated-orcid":false,"given":"Jes\u00fas","family":"Rivera-Nieves","sequence":"additional","affiliation":[{"name":"Gastroenterology Section, San Diego VA Medical Center , La Jolla Village Drive, San Diego, CA , USA"},{"name":"Division of Gastroenterology, Department of Medicine, University of California San Diego , La Jolla, CA , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2023,3,21]]},"reference":[{"key":"2023080117185784100_CIT0001","doi-asserted-by":"crossref","first-page":"1520","DOI":"10.1136\/gut.2010.225482","article-title":"Randomised placebo-controlled trial of rituximab (anti-CD20) in active ulcerative 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