Delcayre A X, Salas F, Mathur S, Kovats K, Lotz M, Lernhardt W
California Institute for Biological Research, La Jolla 92037.
EMBO J. 1991 Apr;10(4):919-26. doi: 10.1002/j.1460-2075.1991.tb08025.x.
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. [125I]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.
干扰素α含有一个与补体片段C3d上的补体受体2型（CR2/CD21）结合位点相似的序列基序。针对C3d上具有CR2结合序列的肽段的抗体，可与携带干扰素α CR2结合基序（第92 - 99位氨基酸残基）的肽段以及重组干扰素α发生反应。源自干扰素α的肽段以及重组干扰素α可抑制C3bi/C3d与伯基特淋巴瘤Raji细胞上的CR2的相互作用。干扰素α与CR2的直接相互作用可被多克隆抗干扰素α、抗CR2和抗C3d肽段抗体以及C3bi/C3d、EB病毒包膜蛋白gp350/220和干扰素所抑制，但不被干扰素γ抑制。[125I]干扰素α与Raji细胞的结合可被多克隆抗干扰素α和抗CR2抗体、具有CR2结合基序的肽段以及部分地被C3bi/C3d所抑制。单克隆抗CR2抗体HB5可阻断干扰素α与Raji细胞的结合，而OKB - 7则不能。因此，CR2或CR2样分子可能是B淋巴细胞上主要的干扰素α受体。
