Hügin A W, Vacchio M S, Morse H C
Laboratory of Immunopathology, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD 20892.
Science. 1991 Apr 19;252(5004):424-7. doi: 10.1126/science.1850169.
The development of an immunodeficiency syndrome of mice caused by a replication-defective murine leukemia virus (MuLV) is paradoxically associated with a rapid activation and proliferation of CD4+ T cells that are dependent on the presence of B cells. The responses of normal spleen cells to B cell lines that express the defective virus indicated that these lines express a cell surface determinant that shares "superantigenic" properties with some microbial antigens and Mls-like self antigens. This antigen elicited a potent proliferative response that was dependent on the presence of CD4+ T cells and was associated with selective expansion of cells bearing V beta 5. This response was markedly inhibited by a monoclonal antibody specific for the MuLV gag-encoded p30 antigen.
由复制缺陷型鼠白血病病毒(MuLV)引起的小鼠免疫缺陷综合征的发展,矛盾的是,与依赖B细胞存在的CD4 + T细胞的快速激活和增殖有关。正常脾细胞对表达缺陷病毒的B细胞系的反应表明,这些细胞系表达一种细胞表面决定簇,该决定簇与某些微生物抗原和Mls样自身抗原具有“超抗原”特性。这种抗原引发了一种强烈的增殖反应,该反应依赖于CD4 + T细胞的存在,并与携带Vβ5的细胞的选择性扩增有关。这种反应被针对MuLV gag编码的p30抗原的单克隆抗体显著抑制。