The life and death of epithelia during inflammation: lessons learned from the gut
2012 (English)In: Annual Review of Pathology, ISSN 1553-4006, E-ISSN 1553-4014, Vol. 7, p. 35-60Article in journal (Refereed) Published
Abstract [en]
Epithelial cells form protective barriers that physically separate an organism from the outside world. Rather than being merely static, impregnable shields, epithelia are highly dynamic structures that can adjust their proliferation, differentiation, and death in response to intrinsic and extrinsic signals. The advantages as well as pitfalls of this flexibility are highlighted in inflammatory disorders such as inflammatory bowel diseases and psoriasis, which are characterized by a chronically dysregulated homeostasis of the epithelium. In recent years, it has become increasingly apparent that epithelial cells communicate with their surroundings through converging, integrated signaling cascades and that even minor alterations in these pathways can have dramatic pathologic consequences. In this review, we discuss how inflammatory cytokines and other signaling molecules, directly or through cross talk, regulate epithelial homeostasis in the intestine, and we highlight parallels and differences in a few other organs.
Place, publisher, year, edition, pages
ANNUAL REVIEWS, 2012. Vol. 7, p. 35-60
Keywords [en]
inflammatory bowel diseases, homeostasis, proliferation, apoptosis, differentiation
National Category
Cell and Molecular Biology
Identifiers
URN: urn:nbn:se:liu:diva-141662DOI: 10.1146/annurev-pathol-011811-120905ISI: 000301837300002PubMedID: 21838548Scopus ID: 2-s2.0-84856940669ISBN: 1553-4014 (Electronic) 1553-4006 (Linking) OAI: oai:DiVA.org:liu-141662DiVA, id: diva2:1149709
Note
Koch, Stefan Nusrat, Asma eng DK 055679/DK/NIDDK NIH HHS/ DK 059888/DK/NIDDK NIH HHS/ DK 089763/DK/NIDDK NIH HHS/ Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Review 2011/08/16 06:00 Annu Rev Pathol. 2012;7:35-60. doi: 10.1146/annurev-pathol-011811-120905. Epub 2011 Aug 12.
2017-10-162017-10-162018-01-13Bibliographically approved