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Originally published online as doi:10.1189/jlb.0105047 on November 10, 2005

Published online before print November 10, 2005
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(Journal of Leukocyte Biology. 2005;78:1106-1117.)
© 2005 by Society for Leukocyte Biology

Fas receptor signaling is requisite for B cell differentiation

Valérie Pasqualetto*, Florence Vasseur*, Flora Zavala{dagger}, Elke Schneider{ddagger} and Sophie Ezine*,1

* INSERM U.591, Institut Necker, Paris, France; and
{dagger} 1NSERM U580 and
{ddagger} CNRS UMR 8147, Hôpital Necker, Paris, France

1Correspondence: INSERM U.591, Institut Necker, 156 rue de Vaugirard, 75730 Paris, Cedex 15, France. E-mail: ezine{at}necker.fr

The Fas/Fas ligand (FasL) pathway has been largely implicated in the homeostasis of mature cells. However, it is still unclear whether it plays a role at the progenitor level. To address this issue, we created chimeric mice by transferring C57BL/6 bone marrow (BM) cells of the lpr (Fas–FasL+) or gld (Fas+FasL–) genotype into Rag-2–/– hosts of the same genetic background. In this model, the consequences of a deficient Fas/FasL pathway on lymphoid differentiation could be evaluated without endogenous competition. Analysis of the chimerism revealed a differential sensitivity of hematopoietic lineages to the lack of Fas receptor signaling. While donor-derived myelo-monocytic cells were similarly distributed in all chimeric mice, mature B cells were deleted in the BM and the spleen of lpr chimera, leading to the absence of the marginal zone (MZ) as detected by immunohistology. In contrast, B cell hematopoiesis was complete in gld chimera but MZ macrophages undetectable. These defects suggest a direct and determinant dual role of FasL regulation in negative selection of B cells and in maintenance of the MZ.

Key Words: FasL • gld • lpr • marginal zone