| First Author | Bonardelle D | Year | 2005 |
| Journal | J Leukoc Biol | Volume | 78 |
| Issue | 5 | Pages | 1052-9 |
| PubMed ID | 16204618 | Mgi Jnum | J:102764 |
| Mgi Id | MGI:3608046 | Doi | 10.1189/jlb.0904536 |
| Citation | Bonardelle D, et al. (2005) B lymphocytes mediate Fas-dependent cytotoxicity in MRL/lpr mice. J Leukoc Biol 78(5):1052-1059 |
| abstractText | The Fas/Fas ligand (FasL) pathway is one of the two major effector mechanisms of T cell-mediated cytotoxicity. To prevent nonspecific killing by lymphoid cells, FasL expression on the cell surface of immune effector cells is strictly regulated. However, MRL/lpr autoimmune-prone mice massively overexpress FasL on their T lymphocytes, which render them able to kill Fas(+) targets in vitro and in vivo. It is surprising that we show in the present work that B lymphocytes purified from MRL/lpr spleen cells express FasL to the same extent as T cells at the mRNA and protein level. These B cells are potent cytotoxic effectors against Fas(+) but not Fas(-) targets. The B lymphocyte effectors were used ex vivo without any in vitro activation by B cell stimuli. Furthermore, we found that MRL/lpr B lymphocytes have the same cytotoxic potential as natural killer cells, which have been characterized as potent, Fas-mediated, cytotoxic effectors. The level of membrane-anchored FasL increases with the size of the B cell and cell-surface activation marker CD69 expression, indicating that the expression of FasL is up-regulated in parallel with the activation state of the B cell. The activated B cell population contained the major cytotoxic activity, and a minor part was associated with CD138/Syndecan-1(+) plasma cells. |
