ArticleCell death & disease2016
Granzyme M has a critical role in providing innate immune protection in ulcerative colitis.
Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
13 citing papers in PubMed, 17 citations in OpenAlex.
- The Serine Protease-Serine Protease Inhibitor Regulatory Network in Inflammatory Bowel Disease: From Molecular Mechanisms to Novel Therapeutic Horizons.Journal of advanced research · 2026Review
- Cytotoxic CD4 T Cells: Dual Agents in HIV-1 Pathogenesis and Persistence.Current HIV/AIDS reports · 2026Review
- A chemiluminescence assay targeting granzyme A activity for monitoring inflammatory bowel disease.Nature biomedical engineering · 2026Article
- Proteases in intestinal health and disease.Nature reviews. Gastroenterology & hepatology · 2026Review
- CD8Journal of inflammation research · 2025Article
- scSTEM: clustering pseudotime ordered single-cell data.Genome biology · 2022Article
- Granzymes-Their Role in Colorectal Cancer.International journal of molecular sciences · 2022Review
- Identification of diagnostic signatures in ulcerative colitis patients via bioinformatic analysis integrated with machine learning.Human cell · 2022Article
- Review
- Granzyme A Stimulates pDCs to Promote Adaptive Immunity via Induction of Type I IFN.Frontiers in immunology · 2019Article
- Screening of genes associated with inflammatory responses in the endolymphatic sac reveals underlying mechanisms for autoimmune inner ear diseases.Experimental and therapeutic medicine · 2018Article
- Regulation of intestinal permeability: The role of proteases.World journal of gastroenterology · 2017Review
- A novel proinflammatory role for granzyme A.Cell death & disease · 2017Article
Corrections and comments
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Authors and funding
16 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammatory bowel disease (IBD) is an immunoregulatory disorder, associated with a chronic and inappropriate mucosal immune response to commensal bacteria, underlying disease states such as ulcerative colitis (UC) and Crohn's disease (CD) in humans. Granzyme M (GrzM) is a serine protease expressed by cytotoxic lymphocytes, in particular natural killer (NK) cells. Granzymes are thought to be involved in triggering cell death in eukaryotic target cells; however, some evidence supports their role in inflammation. The role of GrzM in the innate immune response to mucosal inflammation has never been examined. Here, we discover that patients with UC, unlike patients with CD, display high levels of GrzM mRNA expression in the inflamed colon. By taking advantage of well-established models of experimental UC, we revealed that GrzM-deficient mice have greater levels of inflammatory indicators during dextran sulfate sodium (DSS)-induced IBD, including increased weight loss, greater colon length reduction and more severe intestinal histopathology. The absence of GrzM expression also had effects on gut permeability, tissue cytokine/chemokine dynamics, and neutrophil infiltration during disease. These findings demonstrate, for the first time, that GrzM has a critical role during early stages of inflammation in UC, and that in its absence colonic inflammation is enhanced.
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Registered trials
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