Fibroblasts regulate the switch from acute resolving to chronic persistent inflammation.
By C. Buckley, D. Pilling, J. Lord, A. Akbar, D. Scheel-Toellner, M. Salmon. Trends in immunology, 2001
640 citations recorded by the source corpus.
Subfields: Immunology
View Paper: https://www.semanticscholar.org/paper/a79ffc38c890838b85c7c88d47927575633b74c1
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In Immunology
Citations in the corpus
- Interleukin-6 and chronic inflammation (2006, background): “by local leucocyte recruitment, death and migration [19].”
- Synovial fibroblasts spread rheumatoid arthritis to unaffected joints (2009, background): “RASFs contribute primarily to the progression of the disease by attaching to, invading into and degrading cartilage and bon”
- Inflammation, a Key Event in Cancer Development (2006, background): “The inflammation is precisely timed; however, the aberrations in the apoptosis and phagocytosis of in situ inflammatory cells may lead to an unresolved chronic inflammation (219, 220).”
- Cancer-Associated Fibroblasts Are Activated in Incipient Neoplasia to Orchestrate Tumor-Promoting Inflammation in an NF-kappaB-Dependent Manner. (2010, background): “It has also been suggested that fibroblasts mediate the transition from acute to chronic inflammation by inappropriately providing recruitment, survival, and retention signals to infiltrating leukocytes, thus inhibiting the normal resolution of inflammation (Buckley et al., 2001; Smith et al., 1997)”
- Resolution of inflammation: state of the art, definitions and terms (2006, background): “Evidence now exists that such stromal cells can determine the nature and duration of leukocyte infiltrates (20).”