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Published online before print October 4, 2005
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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0904536

Received for publication September 20, 2004.
Revised July 9, 2005.
Accepted for publication July 15, 2005.

Article

B lymphocytes mediate Fas-dependent cytotoxicity in MRL/lpr mice

Danielle Bonardelle *, Karim Benihoud {dagger}{ddagger}, Nicole Kiger {sect}, and Pierre Bobé *{ddagger}@

*CNRS UPR 9045, Villejuif, France; {dagger}CNRS/Institut Gustave Roussy, UMR 8121, Villejuif, France; {ddagger}Université Paris-Sud, Orsay, France; and {sect}INSERM U 267, Villejuif, France

@ To whom correspondence should be addressed. E-mail: bobe{at}infobiogen.fr.


  Abstract

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/lymphoproliferation (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.

Key Words: activated B cell • Fas ligand • CD69 • autoimmunity




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[Abstract] [Full Text] [PDF]


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