Fas receptor expression on B-lineage cells.
Mice homozygous for the lpr mutation have B and T cell defects and develop autoantibodies, suggesting that lpr plays a role in their genesis. The lpr defect has been identified as a mutation in the apoptosis-associated Fas receptor (FasR) gene. To begin to define the role of FasR in B cells, we have surveyed FasR expression on B-lineage cells from early progenitors in the bone marrow through their maturation in the periphery. Contrary to some reports, we found that FasR is expressed on B cells at all stages of their development and is highest on germinal center B cells. FasR is not expressed on lpr!lpr-derived cells. These data are consistent with the idea that lpr/lpr mice have an intrinsic B cell defect that may be manifested in developing as well as peripheral B cells. An unexpected finding is that B-1 (CD5) B cells do not constitutively express FasR: FasR becomes detectable on B-1 B cells only after activation.
D000818:Animals; D001402:B-Lymphocytes / Q000378:metabolism*; D001854:Bone Marrow Cells; D002454:Cell Differentiation / Q000502:physiology; D053222:Fas Ligand Protein; D008198:Lymph Nodes / Q000166:cytology; D008562:Membrane Glycoproteins / Q000096:biosynthesis*; D051379:Mice; D008807:Mice, Inbred BALB C; D008817:Mice, Mutant Strains; D010529:Peritoneal Cavity / Q000166:cytology; D013154:Spleen / Q000166:cytology; D019014:fas Receptor / Q000096:biosynthesis
D053222:Fas Ligand Protein; C505658:Fasl protein, mouse; D008562:Membrane Glycoproteins; D019014:fas Receptor