Gilmore G L, Cowing C, Mosier D E
Division of Immunology, Medical Biology Institute, La Jolla, California 92037.
J Immunol. 1993 Jan 1;150(1):185-9.
T cell recognition of viral superantigens has been postulated to contribute to the pathogenesis of the immunodeficiency disease induced in mice by infection with the LP-BM5 murine leukemia virus complex. A candidate superantigen has been identified in the B cell lymphoma line B6-1710 derived from an LP-BM5-infected C57BL/6 (H-2b) mouse. We have asked whether the stimulatory activity expressed by B6-1710 behaves as a superantigen by assessing the ability of T cells from fully allogeneic H-2b-->H-2d SCID chimeric mice to respond to the line. T cells from allochimeric mice failed to respond to B6-1710, whereas they responded normally to Staphylococcus enterotoxin B, a well characterized superantigen. Despite this finding, allochimeric mice were fully susceptible to the immune deficiency disease induced by LP-BM5 virus infection. These findings show that the role of superantigen expression in retrovirus-induced immune deficiency disease remains to be defined.
T细胞对病毒超抗原的识别被认为与感染LP - BM5小鼠白血病病毒复合体诱导的小鼠免疫缺陷病的发病机制有关。在源自LP - BM5感染的C57BL / 6（H - 2b）小鼠的B细胞淋巴瘤系B6 - 1710中已鉴定出一种候选超抗原。我们通过评估完全异基因的H - 2b→H - 2d SCID嵌合小鼠的T细胞对该细胞系的反应能力，来探究B6 - 1710所表达的刺激活性是否表现为超抗原。异基因嵌合小鼠的T细胞对B6 - 1710无反应，而它们对特征明确的超抗原——葡萄球菌肠毒素B反应正常。尽管有这一发现，但异基因嵌合小鼠对LP - BM5病毒感染诱导的免疫缺陷病仍完全易感。这些发现表明，超抗原表达在逆转录病毒诱导的免疫缺陷病中的作用仍有待确定。
