Jacobson Amanda C, Weis Janis J, Weis John H
Division of Cell Biology and Immunology, Department of Pathology, University of Utah School of Medicine, Salt Lake City, UT 84132, USA.
Mol Immunol. 2009 Apr;46(7):1488-93. doi: 10.1016/j.molimm.2008.12.030. Epub 2009 Feb 7.
Complement receptor proteins CR2 (CD21) and CR1 (CD35) have been identified as components of the murine B cell co-receptor complex. Gene expression profiles between naïve WT, C3-/-, and CD21/35-/- B cells demonstrate enhanced expression of a Ca(2+)-modulating gene, Pcp4, in WT mice compared to the complement-deficient animals. Increased expression of Pcp4 is also coincident with B cell maturation into end stage phenotypes. Prolonged activation of B cells via cross-linking of the BCR (but not CR1/CR2 alone) leads to increased expression of Pcp4 and suppressed Ca(2+) release. In total these data demonstrate that the expression of Pcp4 in naïve resting mature B cells is dependent upon tonic stimulation from the CR1/CR2 proteins via a C3 ligand, and that antigen specific B cell activation can also elevate Pcp4 expression that is coincident with suppression of calcium-dependent responses.
补体受体蛋白CR2(CD21)和CR1(CD35)已被鉴定为小鼠B细胞共受体复合物的组成部分。幼稚野生型、C3-/-和CD21/35-/- B细胞之间的基因表达谱表明,与补体缺陷动物相比,野生型小鼠中一种钙调节基因Pcp4的表达增强。Pcp4表达的增加也与B细胞成熟为终末表型同时发生。通过BCR交联(但不单独通过CR1/CR2)对B细胞进行长时间激活会导致Pcp4表达增加和Ca(2+)释放受抑制。这些数据总体表明,幼稚静止成熟B细胞中Pcp4的表达依赖于通过C3配体由CR1/CR2蛋白产生的张力刺激,并且抗原特异性B细胞激活也可提高Pcp4表达,这与钙依赖性反应的抑制同时发生。