C3 synthetic peptides support growth of human CR2-positive lymphoblastoid B cells.
C3 synthetic peptides support growth of human CR2-positive lymphoblastoid B cells.
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C3 合成肽支持人类 CR2 阳性淋巴母细胞 B 细胞的生长。
作者：
C. Servis;John D Lambris
通过使用合成肽和CR 2阳性细胞系分析导致人B细胞活化的CR 2型（CR 2）-配体相互作用的性质。C的第三组分（C3）支持人淋巴母细胞样B细胞在含有人转铁蛋白的无血清培养基中生长。这种作用被特异性抑制C3 d与CR2结合的C3 d抗体（mAb 130）抑制，但不被其他抗C3 mAb抑制。与C3 d、P28（残基1187-1214）或多价P13 [1202-1214）4-模板）上的CR 2结合位点对应的合成肽以与C3相似的方式支持CR 2阳性人类淋巴母细胞系的增殖反应，并且该反应可被抗CR 2 mAb OKB 7抑制。对C3或肽的增殖反应是剂量依赖性的，并且需要60倍更高浓度的P28肽来诱导与C3相同水平的增殖。这种生长刺激仅在表达CR2的细胞系Raji和Daudi上观察到，而在CR2阴性伯基特淋巴瘤细胞系Rael和单核细胞系U937上未观察到。与P28和P13模板的刺激作用相反，单体P14（1201-1214）不能支持这些细胞系的生长。然而，该肽抑制了CR 2阳性细胞系对C3、P28和多价-P13的增殖反应，因此表明CR 2受体的交联对于B细胞增殖是必需的。另一种肽E12（来自糖蛋白（GP）350，主要的EBV外膜GP）与P14显示出高度相似性，也抑制Raji细胞的增殖反应，表明GP 350上的该片段参与EBV与CR2的相互作用。讨论了使用上述肽以及其他具有“定制”结构的肽研究C3多功能作用的可能性。
The nature of CR type 2 (CR2)-ligand interactions which leads to the activation of human B cells was analyzed by using synthetic peptides and CR2-positive cell lines. The third component of C (C3) supported the growth of human lymphoblastoid B cells in serum-free medium containing human transferrin. This effect was inhibited by an antibody to C3d (mAb 130) which specifically inhibits C3d binding to CR2, but not by other anti-C3 mAb. Synthetic peptides corresponding to the CR2-binding site on C3d, P28 (residues 1187-1214) or multivalent P13 [1202-1214)4-template), supported the proliferative response of CR2-positive human lymphoblastoid lines in a similar way as C3 and this response could be inhibited by the anti-CR2 mAb OKB7. The proliferative response to C3 or peptides was dose dependent and a 60-fold higher concentration of P28 peptide was required to induce the same level of proliferation as C3. This stimulation of growth was observed only on CR2 expressing cell lines Raji and Daudi, and not on the CR2-negative Burkitt lymphoma cell line Rael and the monocytic cell line U937. In contrast to the stimulatory effect of P28 and P13-template, monomeric P14 (1201-1214) was not able to support the growth of these cell lines. This peptide, however, inhibited the proliferative response of the CR2-positive lines to C3, P28, and multivalent-P13, thus indicating that cross-linking of the CR2 receptor is necessary for B cell proliferation. Another peptide, E12 (from glycoprotein (GP)350, the major EBV outer membrane GP) which shows a high degree of similarity with P14, also inhibited the proliferative response of Raji cells, suggesting that this segment on GP350 is involved in the interaction of EBV with CR2. The possibility of using the above peptides as well as other peptides with "tailor-made" structure in studying the multifunctional role of C3 is discussed.
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DOI：
10.1007/978-1-4757-4862-8_4
发表时间：
1984
期刊：
Contemporary topics in immunobiology
影响因子：
--
作者：
Hugli,TE;Morgan,EL
通讯作者：
Morgan,EL
Epstein Barr 病毒/C3d 受体 (CR2) 的生化和抗原分析。
DOI：
--
发表时间：
1986
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Siaw,MF;Nemerow,GR;Cooper,NR
通讯作者：
Cooper,NR
CR2 配体调节人 B 细胞活化。
DOI：
--
发表时间：
1988
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Bohnsack,JF;Cooper,NR
通讯作者：
Cooper,NR
针对 B 淋巴细胞膜（CR2 受体）的 140,000 mol wt 糖蛋白的单克隆抗体可在体外启动 B 细胞增殖。
影响因子：
20.3
作者：
Wilson,BS;Platt,JL;Kay,NE
通讯作者：
Kay,NE
人 B 细胞分化过程中 C3d 受体的表达：使用 HB-5 单克隆抗体进行免疫荧光分析。
DOI：
--
发表时间：
1984
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Tedder,TF;Clement,LT;Cooper,MD
通讯作者：
Cooper,MD