POSSIBLE ROLE OF CD5+ B-CELLS EXPRESSING CD23 IN MEDIATING THE ELEVATION OF SERUM-SOLUBLE CD23 IN PATIENTS WITH RHEUMATOID-ARTHRITIS
POSSIBLE ROLE OF CD5+ B-CELLS EXPRESSING CD23 IN MEDIATING THE ELEVATION OF SERUM-SOLUBLE CD23 IN PATIENTS WITH RHEUMATOID-ARTHRITIS
复制标题
DOI：
10.1159/000236485
复制
发表时间：
1993-01-01
影响因子：
2.8
通讯作者：
YAMADA, A
中科院分区：
文献类型：
--
作者：
IKIZAWA, K;YANAGIHARA, Y;YAMADA, A
由于类风湿关节炎(RA)等自身免疫性疾病患者血清sCD23/Fc epsilon RII(SCD23)水平明显升高，探讨了RA患者sCD23升高的可能机制。与血清sCD23升高相一致，患者中CD23+B细胞比例较高；这与Fc epsilon RIIA mRNA表达增强有关。在37℃培养条件下，患者外周血单个核细胞自发地向培养上清液中释放高水平的sCD23，而其B细胞上CD23的表达即使在培养后也保持不变。斑点印迹分析进一步表明，与正常对照组相比，RA患者自发培养后Fc epsilon RIIA mRNA没有完全消失。此外，患者加入放线菌酮后，sCD23的释放显著减少。放线菌酮对CD5+CD5+细胞自发表达CD23有抑制作用，但对CD5-B细胞表达无明显影响。但对脐血CD5+细胞和CD5-B细胞CD23的消失无明显影响。这些结果有力地提示，类风湿关节炎患者CD5+B细胞可能被Fc epsilon RIIA mRNA持续表达导致CD23加速周转，进而导致sCD23释放增加的某些机制特异性激活。
Since increased levels of serum soluble CD23/Fc epsilon RII (sCD23) were evidently demonstrated in patients with autoimmune diseases such as rheumatoid arthritis (RA), the possible mechanisms responsible for the elevation of serum sCD23 were investigated in RA patients. In keeping with increased serum sCD23, high proportion of CD23+ B cells was detected in the patients; this was associated with the enhanced expression of only Fc epsilon RIIa mRNA. Upon incubation at 37-degrees-C, peripheral blood mononuclear cells of the patients spontaneously released high levels of sCD23 into the culture supernatant, while the CD23 expression on their B cells was considerably maintained even after the culture. Dot blot analysis further revealed that in contrast to normal subjects, RA patients showed no complete disappearance of Fc epsilon RIIa mRNA after the spontaneous culture. In addition, sCD23 release was significantly reduced in the patients by the addition of cycloheximide. It was also found that cycloheximide exerted the inhibitory influence on the spontaneous culture-mediated expression of CD23 on CD5+ but not CD5- B cells of the patients. However, the disappearance of CD23 from CD5+ as well as CD5- B cells of cord blood samples was unaffected by the agent. These results strongly suggest that CD5+ B cells of RA patients may be specifically activated by some mechanisms responsible for the persistent expression of Fc epsilon RIIa mRNA leading to the accelerated turnover of CD23 and in turn the increased release of sCD23.