Monoclonal antibodies to the human C3b/C4b receptor (CR1) enhance specific B cell differentiation.
Monoclonal antibodies to the human C3b/C4b receptor (CR1) enhance specific B cell differentiation.
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人类 C3b/C4b 受体 (CR1) 的单克隆抗体可增强特异性 B 细胞分化。
DOI：
10.4049/jimmunol.138.9.2988
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发表时间：
1987
影响因子：
4.4
通讯作者：
M. Kazatchkine
中科院分区：
文献类型：
--
作者：
L. Weiss;J. Delfraissy;A. Vazquez;C. Wallon;P. Galanaud;M. Kazatchkine
在第7天的斑块形成细胞试验中，将针对人C3b/C4b受体（CR1）的单克隆抗体添加到外周血淋巴细胞培养物中，在与聚丙烯酰胺珠结合的次优量TNP存在的情况下，特异性抗TNP反应增强了150至400%。抗cr1抗体同样增强了抗荧光素抗体反应。增强仅发生在相关抗原存在的情况下。除了针对其他B细胞表面抗原的单克隆抗体或与抗cr1抗体相同亚类的抗t细胞抗体外，未观察到对抗tnp反应的增强作用。单独抗cr1抗体不能诱导非特异性B细胞增殖，也不能在B细胞生长因子存在的情况下为B细胞提供增殖的第一信号。抗cr1抗体不增强B细胞对pha刺激的T细胞、半纯化的BCGF 20kd、BCGF 50kd或存在抗mu的重组IL 2的生长因子的非特异性增殖反应。在这方面，抗cr1抗体的作用不同于抗cr2抗体，后者与B细胞激活的早期阶段相互作用。相反，当提供可溶性T细胞因子时，抗cr1抗体在缺乏T细胞的情况下增强了抗原活化B细胞的特异性分化。使用两种来源的分化因子，MLA-144上清或从pha刺激的T细胞中提取30至15 KD的部分，均可获得类似的结果。这些结果表明，无论T细胞是由完整的T细胞还是由T细胞衍生的分化因子提供帮助，触发B细胞上的CR1通过增强B细胞分化，积极调节对低剂量抗原的特异性抗体反应。
The addition of monoclonal antibodies against the human C3b/C4b receptor (CR1) to cultures of peripheral blood lymphocytes in the presence of suboptimal amounts of TNP bound to polyacrylamide beads enhanced by 150 to 400% the specific anti-TNP response, as measured by a plaque-forming cell assay on day 7. Anti-CR1 antibodies similarly enhanced the anti-fluorescein antibody response. Enhancement only occurred in cultures performed in the presence of the relevant antigen. No enhancing effect on the anti-TNP response was observed on addition to cultures of monoclonal antibodies directed against other surface antigens of B cells or an anti-T cell antibody of the same subclass as that of anti-CR1 antibodies. Anti-CR1 antibodies alone did not induce nonspecific B cell proliferation and did not provide B cells with a first signal for proliferation in the presence of a source of B cell growth factors. Anti-CR1 antibodies did not enhance the nonspecific proliferative response of B cells to growth factors derived from PHA-stimulated T cells, semi-purified BCGF 20 KD, BCGF 50 KD, or recombinant IL 2 in the presence of anti-mu. In this respect, the effect of anti-CR1 antibodies differs from that of anti-CR2 antibodies which interact with early stages of B cell activation. In contrast, anti-CR1 antibodies enhanced specific differentiation of antigen-activated B cells in the absence of T cells when soluble T cell factors were provided. Similar results were obtained by using either of two sources of differentiation factors, the MLA-144 supernatant or a 30 to 15 KD fraction from PHA-stimulated T cells. These results indicate that triggering of CR1 on B cells positively regulates the specific antibody response to low doses of antigen by enhancing B cell differentiation whether T cell help is provided by intact T cells or by T cell-derived differentiation factors.