| First Author | Zhang H | Year | 2013 |
| Journal | Clin Exp Immunol | Volume | 173 |
| Issue | 3 | Pages | 473-9 |
| PubMed ID | 23617623 | Mgi Jnum | J:200639 |
| Mgi Id | MGI:5508980 | Doi | 10.1111/cei.12126 |
| Citation | Zhang H, et al. (2013) Hepatic B cells are readily activated by Toll-like receptor-4 ligation and secrete less interleukin-10 than lymphoid tissue B cells. Clin Exp Immunol 173(3):473-9 |
| abstractText | B cells perform various immunological functions that include production of antibody, presentation of antigens, secretion of multiple cytokines and regulation of immune responses mainly via their secretion of interleukin (IL)-10. While the liver is regarded both as an important immune organ and a tolerogenic environment, little is known about the functional biology of hepatic B cells. In this study we demonstrate that, following lipopolysaccharide (LPS) stimulation in vivo, normal mouse hepatic B cells rapidly increase their surface expression of CD39, CD40, CD80 and CD86, and produce significantly elevated levels of proinflammatory interferon (IFN)-gamma, IL-6 and tumour necrosis factor (TNF)-alpha compared with splenic B cells. Moreover, LPS-activated hepatic B cells produce very low levels of IL-10 compared with activated splenic B cells that produce comparatively high levels of this immunosuppressive cytokine. Splenic, but not hepatic, B cells inhibited the activation of liver conventional myeloid dendritic cells (mDCs). Furthermore, compared with the spleen, the liver exhibited significantly smaller proportions of B1a and marginal zone-like B cells, which have been shown to produce IL-10 upon LPS stimulation. These data suggest that, unlike in the spleen, IL-10-producing regulatory B cells in the liver are not a prominent cell type. Consistent with this, when compared with liver conventional mDCs from B cell-deficient mice, those from B cell-competent wild-type mice displayed enhanced expression of the cell surface co-stimulatory molecule CD86, greater production of proinflammatory cytokines (IFN-gamma, IL-6, IL-12p40) and reduced secretion of IL-10. These findings suggest that hepatic B cells have the potential to initiate rather than regulate inflammatory responses. |
