Sharujan Suthakaran
Research Subjects
Research Interests
Sharujan Suthakaran has a total of 44 co-authors. Here are the top co-authors by number of shared publications:
- Adrian Feile
Department of Dermatology University Hospital Tübingen Tübingen Germany
1 shared publication - Alexander S. Mosig
Institute of Biochemistry II, Jena University Hospital, Jena, Germany
1 shared publication Alissa Walsh
1 shared publication- Alistair Easton
Department of Oncology, University of Oxford, Oxford, United Kingdom
1 shared publication Bin Li
1 shared publicationBruce George
1 shared publication
Latest Publications
- Open Access
- 12 August 2026
- Published by Springer Nature in Nature Immunology
- Vol. 27 (9) , 1954-1968
Epigenetic modulation of stromal cell states underpins pathological tissue niches in Crohn’s disease
Stromal cell states are altered in active Crohn’s disease (CD), but their origin and phenotypic stability are unknown. Using single-cell spatial transcriptomics, RNA sequencing and ATAC sequencing of ~2,500,000 cells, we map 18 distinct stromal cell states within their cellular and cytokine signaling environments in human full-thickness CD bowel. Inflammatory fibroblasts (IFs) reside in immune cell-rich mucosal ulcers and are induced through combinatorial cytokine exposure suppressing submucosal universal fibroblast programs. The IF state is stabilized through transcription factor (TF) activity of GLI3, TWIST1, ETV4, PRDM1 and RELB, and does not spontaneously revert; however, histone deacetylase inhibition destabilizes the IF state, preventing IF secretome-induced epithelial transmigration and activation of neutrophils. The IF open chromatin configuration is distinct from that of fibrotic contractile stroma, which populate adjoining immune-depleted submucosal fibrotic niches. These findings show that microenvironments in pathological tissue niches shape open chromatin configuration of stromal states that are amenable to modulation by epigenetic modifiers.
- 12 August 2026
- Published by Springer Nature in Nature Immunology
- Vol. 27 (9) , 1954-1968
Open AccessEpigenetic modulation of stromal cell states underpins pathological tissue niches in Crohn’s disease
Stromal cell states are altered in active Crohn’s disease (CD), but their origin and phenotypic stability are unknown. Using single-cell spatial transcriptomics, RNA sequencing and ATAC sequencing of ~2,500,000 cells, we map 18 distinct stromal cell states within their cellular and cytokine signaling environments in human full-thickness CD bowel. Inflammatory fibroblasts (IFs) reside in immune cell-rich mucosal ulcers and are induced through combinatorial cytokine exposure suppressing submucosal universal fibroblast programs. The IF state is stabilized through transcription factor (TF) activity of GLI3, TWIST1, ETV4, PRDM1 and RELB, and does not spontaneously revert; however, histone deacetylase inhibition destabilizes the IF state, preventing IF secretome-induced epithelial transmigration and activation of neutrophils. The IF open chromatin configuration is distinct from that of fibrotic contractile stroma, which populate adjoining immune-depleted submucosal fibrotic niches. These findings show that microenvironments in pathological tissue niches shape open chromatin configuration of stromal states that are amenable to modulation by epigenetic modifiers.