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Attenuated liver fibrosis in the absence of B cells

✍ Scribed by Andrew P. Holt; Zania Stamataki; David H. Adams

Publisher: John Wiley and Sons
Year: 2006
Tongue: English
Weight: 461 KB
Volume: 43
Category: Article
ISSN: 0270-9139
DOI: 10.1002/hep.21155

No coin nor oath required. For personal study only.

✦ Synopsis

Analysis of mononuclear cells in the adult

mouse liver revealed that B cells represent as much as half of the intrahepatic lymphocyte population. Intrahepatic B cells (IHB cells) are phenotypically similar to splenic B2 cells but express lower levels of CD23 and CD21 and higher levels of CD5. IHB cells proliferate as well as splenic B cells in response to anti-IgM and LPS stimulation in vitro. VDJ gene rearrangements in IHB cells contain insertions of N,P region nucleotides characteristic of B cells maturing in the adult bone marrow rather than in the fetal liver. To evaluate whether B cells can have an impact on liver pathology, we compared CCl4-induced fibrosis development in B cell-deficient and wild-type mice. CCl4 caused similar acute liver injury in mutant and wild-type mice. However, following 6 weeks of CCl4 treatment, histochemical analyses showed markedly reduced collagen deposition in B cell-deficient as compared with wild-type mice. By analyzing mice that have normal numbers of B cells but lack either T cells or immunoglobulin in the serum, we established that B cells have an impact on fibrosis in an antibody-and T cell-independent manner.

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