IMMUNOLOGY2026™ Conference Recordings For Attendees-CX3CR1+ myeloid cell-intrinsic NOD2 signaling limits Crohn's disease-associated intestinal fibrosis

CX3CR1+ myeloid cell-intrinsic NOD2 signaling limits Crohn's disease-associated intestinal fibrosis

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Video Summary

The speaker presented postdoctoral research on how NOD2 signaling in CXCR1/CCR2-related myeloid cells limits Crohn’s disease-associated intestinal fibrosis. Using a chronic DSS mouse model and single-cell analysis, the study found that NOD2 deficiency worsened inflammation, increased collagen deposition, and promoted fibrotic tissue formation. NOD2-deficient mice showed expansion of inflammatory fibroblasts and a novel mesenchymal “FATE” cell population, along with loss of normal capillaries, increased arteries, and reduced lymphatics. The team also identified a key reduction in pro-restitutive CX3CR1/CD206 macrophages. Deleting NOD2 specifically in CX3CR1 macrophages reproduced the inflammatory and fibrotic phenotype, suggesting these cells normally support tissue repair and restrain mesenchymal drift. Overall, the work suggests NOD2 signaling in CX3CR1 macrophages helps maintain intestinal homeostasis and may protect against Crohn’s-related fibrosis.

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Date April 16, 2026 9:45 AM - 10:00 AM

Room 102

Session Innate Immune Defenses in the Epithelium

Speaker Tapas Mukherjee

Track Innate Immune Responses and Host Defense: Cellular Mechanisms (INC)

Year 2026

Keywords

NOD2 signaling

Crohn’s disease fibrosis

CX3CR1 macrophages

intestinal fibrosis

single-cell analysis

April 16, 2026 9:45 AM - 10:00 AM

102

Innate Immune Defenses in the Epithelium

Tapas Mukherjee

Innate Immune Responses and Host Defense: Cellular Mechanisms (INC)

2026