Inflammatory Bowel Disease

This study shows that loss of SNX27 in intestinal epithelial cells disrupts barrier function and promotes inflammation in mice, with reduced SNX27 expression observed in human IBD.

The paper generates intestinal organoids from pediatric IBD patients and controls to study epithelial phenotypes linked to genetic drivers of the disease, identifying gene expression patterns and pathways associated with inflammation.

The paper identifies an inflammatory secretory progenitor cell state in Crohn's disease patients and shows its epigenetic regulation in stem cells.

This study shows ADAMTS13 deficiency worsens ulcerative colitis by promoting microthrombi formation, mucosal damage, and endothelial dysfunction, with intravital imaging revealing these mechanisms at single-cell resolution.

The paper shows reduced GLP-1+ cell numbers in inflamed intestinal tissues of mice and CD patients, linked to an inflammatory metabolic signature affecting epithelial differentiation.

The paper identifies niColAMs as critical for IBD recovery and shows GIV-NOD2 interaction is essential for microbial sensing and gut homeostasis.

This study investigates how the LRRK2-N2081D variant increases Crohn's disease risk by showing it causes more severe colitis and distinct RAB substrate phosphorylation compared to LRRK2-G2019S.

This study shows that intestinal epithelial PTPN2 limits AIEC colonization by enhancing antimicrobial peptide expression and immune responses.

The paper uses targeted NGS to identify functional SNPs and pathways associated with IBD in GSDs, revealing genetic markers for treatment response.

This study shows that IBD susceptibility increases the risk of ATF6-driven tumorigenesis in a murine model.

This study shows CD131 promotes macrophage infiltration in ulcerative colitis, contributing to disease severity through CCL4-mediated chemotaxis.

This study investigates the role of MAIT cells in a genetically diverse mouse model of spontaneous colitis, finding that MAIT cells drive chronic inflammation and colonic pathology.

This study shows that DR3 signaling promotes Th9 cell pathogenicity in CD-like ileitis by enhancing pro-inflammatory signatures and reducing anti-inflammatory responses.

The paper investigates resistance to JAK inhibitors in UC by analyzing single-cell RNA data from responders and non-responders, identifying hyperactivation of myeloid cells as a key mechanism.

The paper identifies transcriptomic signatures in aphthous ulcers of Crohn's disease, suggesting bacterial invasion initiates inflammation rather than dysbiosis.

The paper compares 13 mouse models of intestinal inflammation with human IBD datasets to identify translatable pathways and introduces a web tool for analyzing these models.

This study shows IFN-gamma induces PANoptosis in intestinal epithelial cells in Crohn's disease, which can be inhibited by the JAK1 inhibitor upadacitinib.

This study integrates multi-omic and multimodal data from IBD patients to identify molecular, histopathological, and clinical features associated with inflammatory bowel diseases.

This study identifies dysregulation of γδ intraepithelial lymphocytes (IELs) before the onset of Crohn's disease-like ileitis in a mouse model.

The paper identifies public TCRB sequences expanded in CD or UC, associated with HLA alleles and antigen-specific immune responses, showing differential expansion in CD compared to UC and healthy controls.

This study shows that baicalein reduces UC recurrence by lowering FcRn expression through the NF-κB pathway in mice.

This study uses spatial biology to identify intestinal and systemic molecular drivers of inflammation in DSS-treated mice, revealing new insights into IBD-related systemic effects.

This study investigates how stem cell transplantation (SCT) restores immune function in refractory Crohn's disease by analyzing immune cell remodeling and HSC heterogeneity using single-cell RNA sequencing and functional assays.

The paper examines monocyte subsets in Crohn's disease patients, finding classical monocytes show an exhaustion profile with increased CD38 and reduced IL-1β production after LPS stimulation.

The paper investigates the relationship between mitochondrial dysfunction and anti-TNF treatment response in ulcerative colitis using both murine and human samples, finding metabolic pathways and mitochondrial homeostasis are involved.

This study shows serotonin reduces inflammation in intestinal tissue by altering monocyte behavior and chemokine expression using a human 3D model.

This study identifies histopathological and molecular features linked to J-pouch failure in IBD patients using single-cell spatial transcriptomics.

This study identifies Fmo5's sex-specific role in goblet cell maturation and mucus barrier formation in the intestine, with severe effects in female mice.

The paper identifies MUC17 as a critical component of the small intestinal glycocalyx that is disrupted in Crohn's disease, leading to bacterial contact and epithelial defects.