Castagnoli Riccardo, Pala Francesca, Subramanian Poorani, Oguz Cihan, Schwarz Benjamin, Lim Ai Ing, Burns Andrew S, Fontana Elena, Bosticardo Marita, Corsino Cristina, Angelova Angelina, Delmonte Ottavia M, Kenney Heather, Riley Deanna, Smith Grace, Ott de Bruin Lisa, Oikonomou Vasileios, Dos Santos Dias Lucas, Fink Danielle, Bohrnsen Eric, Kimzey Cole D, Marseglia Gian Luigi, Alva-Lozada Guisela, Bergerson Jenna R E, Brett Ana, Brigatti Karlla W, Dimitrova Dimana, Dutmer Cullen M, Freeman Alexandra F, Ale Hanadys, Holland Steven M, Licciardi Francesco, Pasic Srdjan, Poskitt Laura E, Potts David E, Dasso Joseph F, Sharapova Svetlana O, Strauss Kevin A, Ward Brant R, Yilmaz Melis, Kuhns Douglas B, Lionakis Michail S, Daley Stephen R, Kong Heidi H, Segre Julia A, Villa Anna, Pittaluga Stefania, Walter Jolan E, Vujkovic-Cvijin Ivan, Belkaid Yasmine, Notarangelo Luigi D
Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.
Bioinformatics and Computational Biosciences Branch, Office of Cyber Infrastructure and Computational Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health , Bethesda, MD, USA.
J Exp Med. 2025 Aug 4;222(8). doi: 10.1084/jem.20241993. Epub 2025 May 2.
Partial RAG deficiency (pRD) can manifest with systemic and tissue-specific immune dysregulation, with inflammatory bowel disease (IBD) in 15% of the patients. We aimed at identifying the immunopathological and microbial signatures associated with IBD in patients with pRD and in a mouse model of pRD (Rag1w/w) with spontaneous development of colitis. pRD patients with IBD and Rag1w/w mice showed a systemic and colonic Th1/Th17 inflammatory signature. Restriction of fecal microbial diversity, abundance of pathogenic bacteria, and depletion of microbial species producing short-chain fatty acid were observed, which were associated with impaired induction of lamina propria peripheral Treg cells in Rag1w/w mice. The use of vedolizumab in Rag1w/w mice and of ustekinumab in a pRD patient were ineffective. Antibiotics ameliorated gut inflammation in Rag1w/w mice, but only bone marrow transplantation (BMT) rescued the immunopathological and microbial signatures. Our findings shed new light in the pathophysiology of gut inflammation in pRD and establish a curative role for BMT to resolve the disease phenotype.
部分RAG缺陷(pRD)可表现为全身和组织特异性免疫失调,15%的患者会出现炎症性肠病(IBD)。我们旨在确定与pRD患者以及自发发生结肠炎的pRD小鼠模型(Rag1w/w)中的IBD相关的免疫病理学和微生物特征。患有IBD的pRD患者和Rag1w/w小鼠表现出全身和结肠Th1/Th17炎症特征。观察到粪便微生物多样性受限、病原菌丰度增加以及产生短链脂肪酸的微生物种类减少,这与Rag1w/w小鼠固有层外周调节性T细胞诱导受损有关。在Rag1w/w小鼠中使用维多珠单抗以及在一名pRD患者中使用乌司奴单抗均无效。抗生素改善了Rag1w/w小鼠的肠道炎症,但只有骨髓移植(BMT)挽救了免疫病理学和微生物特征。我们的研究结果为pRD肠道炎症的病理生理学提供了新的见解,并确立了BMT在解决疾病表型方面的治愈作用。