Ahearn J M, Fischer M B, Croix D, Goerg S, Ma M, Xia J, Zhou X, Howard R G, Rothstein T L, Carroll M C
Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115, USA.
Immunity. 1996 Mar;4(3):251-62. doi: 10.1016/s1074-7613(00)80433-1.
Covalent attachment of activated products of the third component of complement to antigen enhances its immunogenicity, but the mechanism is not clear. This effect is mediated by specific receptors, mCR1 (CD35) and mCR2 (CD21), expressed primarily on B cells and follicular dendritic cells in mice. To dissect the role of mCR1 and mCR2 in the humoral response, we have disrupted the Cr2 locus to generate mice deficient in both receptors. The deficient mice (Cr2-/-) were found to have a reduction in the CD5+ population of peritoneal B-1 cells, although their serum IgM levels were within the range of normal mice. Moreover, Cr2-/- mice had a severe defect in their humoral response to T-dependent antigens that was characterized by a reduction in serum antibody titers and in the number and size of germinal centers within splenic follicles. Reconstitution of the deficient mice with bone marrow from MHC-matched Cr2+/+ donors corrected the defect, demonstrating that the defect was due to B cells themselves. These results indicate an obligatory role of B cell complement receptors in responses of the B cells to protein antigens.
补体第三成分的活化产物与抗原的共价结合增强了其免疫原性，但其机制尚不清楚。这种效应由主要在小鼠B细胞和滤泡树突状细胞上表达的特异性受体mCR1（CD35）和mCR2（CD21）介导。为了剖析mCR1和mCR2在体液反应中的作用，我们破坏了Cr2基因座以产生两种受体均缺陷的小鼠。发现缺陷小鼠（Cr2-/-）腹膜B-1细胞的CD5+群体减少，尽管其血清IgM水平在正常小鼠范围内。此外，Cr2-/-小鼠对T细胞依赖性抗原的体液反应存在严重缺陷，其特征是血清抗体滴度降低以及脾滤泡内生发中心的数量和大小减少。用来自MHC匹配的Cr2+/+供体的骨髓重建缺陷小鼠纠正了该缺陷，表明该缺陷是由于B细胞本身所致。这些结果表明B细胞补体受体在B细胞对蛋白质抗原的反应中起必不可少的作用。
