Fas receptor signaling is requisite for B cell differentiation

Abstract : 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.
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Soumis le : lundi 28 janvier 2019 - 14:24:00
Dernière modification le : jeudi 11 avril 2019 - 16:02:54

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Valérie Pasqualetto, Florence Vasseur, Flora Zavala, Elke Schneider, Sophie Ezine. Fas receptor signaling is requisite for B cell differentiation. Journal of Leukocyte Biology, Society for Leukocyte Biology, 2005, 78 (5), pp.1106-1117. ⟨10.1189/jlb.0105047⟩. ⟨hal-01996498⟩

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