Gareth‐Rhys Jones

The paper identifies molecular signatures of Crohn's disease using scRNA-seq data from terminal ileal biopsies, highlighting key cell types and pathways involved in disease pathogenesis.

The paper shows that monocyte-derived alveolar macrophages (mono-AMs) from different insults follow a conserved differentiation blueprint, while fetal-derived AMs show context-dependent changes.

This study shows TWEAK increases in ulcerative colitis and promotes monocyte activation through non-canonical NF-kB/STAT3 signaling in fibroblasts.

This study identifies three subpopulations of colonic macrophages in mice, showing they persist through inflammation and adapt transcriptionally to aid tissue repair.

The paper shows loss of HMGCS2-mediated ketogenesis in intestinal stem cells impairs mucosal healing in Ulcerative colitis and identifies {beta}HB as a potential therapeutic target.

The paper maps cell-type-specific eQTLs in IBD patients to identify effector genes and mechanisms linking genetic risk to disease.

This study uses single-cell RNA sequencing to analyze immune cell transcriptional profiles in mucosal and circulatory compartments of Crohn's disease patients, revealing tissue-specific inflammation signatures and identifying circulating T cells with mucosal-like features.

The paper identifies inflammation-associated monocytes (IAMs) in IBD and experimental colitis, showing they express ACOD1 to limit cytokine production during inflammation.

This study identifies HLA-DQA1*05 as a genetic risk factor for anti-drug antibody development in Crohn's disease patients treated with anti-TNF therapies.