{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"bioRxiv"}],"indexed":{"date-parts":[[2026,6,24]],"date-time":"2026-06-24T05:48:01Z","timestamp":1782280081046,"version":"3.54.5"},"posted":{"date-parts":[[2025,1,24]]},"group-title":"Immunology","reference-count":119,"publisher":"openRxiv","license":[{"start":{"date-parts":[[2025,1,24]],"date-time":"2025-01-24T00:00:00Z","timestamp":1737676800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/publicdomain\/zero\/1.0\/"}],"funder":[{"name":"NIH","award":["R01-AI141630, UG3TR003355, UG3TR002968, and R01-AI55696"],"award-info":[{"award-number":["R01-AI141630, UG3TR003355, UG3TR002968, and R01-AI55696"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2025,7,31]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                <jats:p>\n                  Single-cell studies have revealed that intestinal macrophages maintain gut homeostasis through the balanced actions of reactive (inflammatory) and tolerant (non-inflammatory) subpopulations. How such balance is impaired in inflammatory bowel diseases (IBD), including Crohn\u2019s disease (CD) and ulcerative colitis (UC), remains unresolved. Here, we define colon-specific macrophage states and reveal the critical role of\n                  <jats:italic>\n                    <jats:underline>n<\/jats:underline>\n                  <\/jats:italic>\n                  on-\n                  <jats:italic>i<\/jats:italic>\n                  nflammatory\n                  <jats:italic>\n                    <jats:underline>c<\/jats:underline>\n                  <\/jats:italic>\n                  olon-\n                  <jats:italic>\n                    <jats:underline>a<\/jats:underline>\n                  <\/jats:italic>\n                  ssociated\n                  <jats:italic>\n                    <jats:underline>m<\/jats:underline>\n                  <\/jats:italic>\n                  acrophages (niColAMs) in IBD recovery. Through trans-scale analyses\u2014integrating computational transcriptomics, proteomics, and\n                  <jats:italic>in vivo<\/jats:italic>\n                  interventional studies\u2014we identified GIV (\n                  <jats:italic>CCDC88A<\/jats:italic>\n                  ) as a key regulator of niColAMs. GIV emerged as the top-ranked gene in niColAMs that physically and functionally interacts with NOD2, an innate immune sensor implicated in CD and UC. Myeloid-specific GIV depletion exacerbates infectious colitis, prolongs disease, and abolishes the protective effects of the NOD2 ligand, muramyl dipeptide, in colitis and sepsis models. Mechanistically, GIV\u2019s C-terminus binds the terminal leucine-rich repeat (LRR#10) of NOD2 and is required for NOD2 to dampen inflammation and clear microbes. The CD-associated\n                  <jats:italic>1007fs<\/jats:italic>\n                  NOD2-variant, which lacks LRR#10, cannot bind GIV\u2014providing critical insights into how this clinically relevant variant impairs microbial sensing and clearance. These findings illuminate a critical GIV-NOD2 axis essential for gut homeostasis and highlight its disruption as a driver of dysbiosis and inflammation in IBD.\n                <\/jats:p>","DOI":"10.1101\/2025.01.21.634180","type":"posted-content","created":{"date-parts":[[2025,1,24]],"date-time":"2025-01-24T17:55:16Z","timestamp":1737741316000},"source":"Crossref","is-referenced-by-count":1,"title":["Distinct Colitis-Associated Macrophages Drive NOD2-Dependent Bacterial Sensing and Gut Homeostasis"],"prefix":"10.64898","author":[{"given":"Gajanan D.","family":"Katkar","sequence":"first","affiliation":[{"name":"Department of Cellular and Molecular Medicine, University of California San Diego, CA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mahitha Shree","family":"Anandachar","sequence":"additional","affiliation":[{"name":"Department of Cellular and Molecular Medicine, University of California San Diego, CA, USA"},{"name":"Department of Pathology, University of 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