EPSTEIN-BARR-VIRUS COMPLEMENT C3D RECEPTOR IS AN INTERFERON-ALPHA RECEPTOR
EPSTEIN-BARR-VIRUS COMPLEMENT C3D RECEPTOR IS AN INTERFERON-ALPHA RECEPTOR
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DOI：
10.1002/j.1460-2075.1991.tb08025.x
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发表时间：
1991-04-01
期刊：
影响因子：
11.4
通讯作者：
LERNHARDT, W
中科院分区：
文献类型：
--
作者：
DELCAYRE, AX;SALAS, F;LERNHARDT, W
干扰素-α 包含与补体片段 C3d 上的补体受体二型 (CR2/CD21) 结合位点相似的序列基序。针对 C3d 上具有 CR2 结合序列的肽的抗体与携带 IFN-α CR2 结合基序（残基 92-99）的肽以及重组 IFN-α 发生反应。 IFN-α 衍生肽以及重组 IFN-α 可抑制伯基特淋巴瘤 Raji 上 C3bi/C3d 与 CR2 的相互作用。 IFN-α 和 CR2 的直接相互作用可被多克隆抗 IFN-α、抗 CR2 和抗 C3d 肽抗体以及 C3bi/C3d、EBV 外壳蛋白 gp350/220 和 IFN 抑制，但不会被 IFN-gamma 抑制。 [I-125]IFN-α 与 Raji 细胞的结合受到多克隆抗 IFN-α 和抗 CR2 抗体、具有 CR2 结合基序的肽以及部分 C3bi/C3d 的抑制。单克隆抗 CR2 抗体 HB5（而非 OKB-7）可阻断 IFN-α 与 Raji 细胞的结合。因此，CR2 或 CR2 样分子可能是 B 淋巴细胞上主要的 IFN-α 受体。
Interferon-alpha contains a sequence motif similar to the complement receptor type two (CR2/CD21) binding site on complement fragment C3d. Antibodies against a peptide with the CR2 binding sequence on C3d react with a peptide carrying the IFN-alpha CR2 binding motif (residues 92-99) and with recombinant IFN-alpha. The IFN-alpha-derived peptide, as well as recombinant IFN-alpha, inhibits C3bi/C3d interaction with CR2 on the Burkitt lymphoma Raji. The direct interaction of IFN-alpha and CR2 is inhibited by polyclonal anti-IFN-alpha, anti-CR2 and anti-C3d peptide antibodies as well as by C3bi/C3d, EBV coat protein gp350/220 and IFN but not by IFN-gamma. [I-125]IFN-alpha binding to Raji cells is inhibited by polyclonal anti-IFN-alpha and anti-CR2 antibodies, by peptides with the CR2 binding motif and partially by C3bi/C3d. Monoclonal anti-CR2 antibody HB5, but not OKB-7, blocks IFN-alpha binding to Raji cells. CR2 or CR2-like molecules may therefore be the major IFN-alpha receptors on B lymphocytes.