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Dendritic cells in liver fibrosis: conductor of the inflammatory orchestra?

✍ Scribed by Costica Aloman; Frank Tacke

Publisher
John Wiley and Sons
Year
2010
Tongue
English
Weight
111 KB
Volume
51
Category
Article
ISSN
0270-9139

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✦ Synopsis

Hepatic fibrosis occurs during most chronic liver diseases and is driven by inflammatory responses to injured tissue. Because DCs are central to modulating liver immunity, we postulated that altered DC function contributes to immunologic changes in hepatic fibrosis and affects the pathologic inflammatory milieu within the fibrotic liver. Using mouse models, we determined the contribution of DCs to altered hepatic immunity in fibrosis and investigated the role of DCs in modulating the inflammatory environment within the fibrotic liver. We found that DC depletion completely abrogated the elevated levels of many inflammatory mediators that are produced in the fibrotic liver. DCs represented approximately 25% of the fibrotic hepatic leukocytes and showed an elevated CD11bþCD8-fraction, a lower B220þ plasmacytoid fraction, and increased expression of MHC II and CD40. Moreover, after liver injury, DCs gained a marked capacity to induce hepatic stellate cells, NK cells, and T cells to mediate inflammation, proliferation, and production of potent immune responses. The proinflammatory and immunogenic effects of fibrotic DCs were contingent on their production of TNF-a. Therefore, modulating DC function may be an attractive approach to experimental therapeutics in fibro-inflammatory liver disease. V

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