Mandik L, Nguyen K A, Erikson J
Wistar Institute, Philadelphia 19104, USA.
Eur J Immunol. 1995 Nov;25(11):3148-54. doi: 10.1002/eji.1830251124.
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.
纯合 lpr 突变的小鼠存在 B 细胞和 T 细胞缺陷，并产生自身抗体，这表明 lpr 在其发生过程中起作用。lpr 缺陷已被确定为凋亡相关 Fas 受体（FasR）基因中的突变。为了开始确定 FasR 在 B 细胞中的作用，我们研究了从骨髓中的早期祖细胞到外周成熟过程中 B 系细胞上 FasR 的表达情况。与一些报道相反，我们发现 FasR 在 B 细胞发育的所有阶段均有表达，并且在生发中心 B 细胞上表达最高。FasR 在 lpr/lpr 来源的细胞上不表达。这些数据与 lpr/lpr 小鼠存在内在 B 细胞缺陷的观点一致，这种缺陷可能在发育中的 B 细胞以及外周 B 细胞中表现出来。一个意外的发现是，B-1（CD5）B 细胞不组成性表达 FasR：FasR 仅在激活后才在 B-1 B 细胞上可检测到。
