{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,16]],"date-time":"2026-07-16T12:23:28Z","timestamp":1784204608562,"version":"3.55.0"},"reference-count":50,"publisher":"American Society of Hematology","issue":"13","content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2026,3,26]]},"abstract":"<jats:sec>\n                    <jats:title>Abstract<\/jats:title>\n                    <jats:p>Intestinal Enterococcus domination has been associated with an increased risk of mortality from acute graft-versus-host disease (GVHD) after allogeneic hematopoietic cell transplantation (allo-HCT), a curative-intent treatment for patients with hematologic malignancies. In this study, we investigated interactions between Enterococcus and the intestinal epithelium as a mechanism to aggravate GVHD. We observed that endogenous intestinal Enterococcus outgrowth was associated with increased GVHD mortality and major histocompatibility complex class II (MHC-II) expression by intestinal epithelial cells in the colon in an MHC-disparate mouse model of GVHD. Monocolonization of nontransplanted gnotobiotic mice with Enterococcus faecalis was sufficient to induce colonic MHC-II expression. Conversely, select species within the genus Enterococcus, as well as a consortium of 4 anaerobic commensal bacteria including Blautia producta, did not affect colonic MHC-II expression in gnotobiotic mice. In addition, E faecalis colonization induced inflammatory responses in CD4+ T cells and natural killer cells from the colonic lamina propria, the 2 main sources of interferon gamma production that drives MHC-II expression in nonprofessional antigen-presenting cells. We further explored the potential therapeutic benefit of establishing colonization resistance against E faecalis through administration of a lantibiotic-producing B producta strain after allo-HCT. Colonization of transplanted mice with a consortium of commensal bacteria containing the lantibiotic-producing B producta strain prevented intestinal Enterococcus domination after transplantation and improved GVHD survival. Our results demonstrate a potential mechanism by which Enterococcus aggravates GVHD through increased MHC-II expression in the intestinal epithelium. Targeting the Enterococcus\u2013epithelium\u2013MHC-II axis thus presents a therapeutic opportunity to prevent lethal GVHD.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1182\/blood.2024028248","type":"journal-article","created":{"date-parts":[[2025,12,29]],"date-time":"2025-12-29T19:05:25Z","timestamp":1767035125000},"page":"1485-1497","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":4,"title":["<i>Enterococcus faecalis<\/i>\n                    induces MHC-II expression by the intestinal epithelium during murine graft-versus-host disease"],"prefix":"10.1182","volume":"147","author":[{"given":"Chi L.","family":"Nguyen","sequence":"first","affiliation":[{"name":"1Department of Immunology, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, NY"},{"name":"2Beckman Research Institute, City of Hope Comprehensive Cancer Center, Duarte, 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