| First Author | Novobrantseva TI | Year | 2005 |
| Journal | J Clin Invest | Volume | 115 |
| Issue | 11 | Pages | 3072-82 |
| PubMed ID | 16276416 | Mgi Jnum | J:102501 |
| Mgi Id | MGI:3607670 | Doi | 10.1172/JCI24798 |
| Citation | Novobrantseva TI, et al. (2005) Attenuated liver fibrosis in the absence of B cells. J Clin Invest 115(11):3072-3082 |
| abstractText | 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 CCl(4)-induced fibrosis development in B cell-deficient and wild-type mice. CCl(4) caused similar acute liver injury in mutant and wild-type mice. However, following 6 weeks of CCl(4) 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. |
