AbstractMice homozygous for thelprmutation have B and T cell defects and develop autoantibodies, suggesting thatlprplays a role in their genesis. Thelprdefect 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 onlpr/lpr‐derived cells. These data are consistent with the idea thatlpr/lprmice 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 a
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