期刊
MUCOSAL IMMUNOLOGY
卷 9, 期 3, 页码 567-582出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/mi.2016.14
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资金
- Medical Research Council
- Edinburgh Gut Immunobiology and Gastroenterology Trustees Fund
- Chief Scientist Office [ETM/75, ETM/137] Funding Source: researchfish
- Crohn's and Colitis UK [M16-1] Funding Source: researchfish
- Medical Research Council [G0601481, G0800675, 1202121, G0901697, G0701898, G0600329, MR/K013386/1, G0800759] Funding Source: researchfish
- MRC [G0600329, MR/K013386/1, G0800675, G0800759, G0601481, G0701898, G0901697] Funding Source: UKRI
Endogenous damage-associated molecular patterns (DAMPs) are released during tissue damage and have increasingly recognized roles in the etiology of many human diseases. The inflammatory bowel diseases (IBD), ulcerative colitis (UC) and Crohn's disease (CD), are immune-mediated conditions where high levels of DAMPs are observed. DAMPs such as calprotectin (S100A8/9) have an established clinical role as a biomarker in IBD. In this review, we use IBD as an archetypal commonchronic inflammatory disease to focus on the conceptual and evidential importance of DAMPsin pathogenesis and why DAMPs represent an entirely new class of targets for clinical translation.
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