Beutner U, McLellan B, Kraus E, Huber B T
Program of Immunology, Sackler School for Graduate Biomedical Sciences, Tufts University School of Medicine, Boston, MA 02111, USA.
Cell Immunol. 1996 Mar 15;168(2):141-7. doi: 10.1006/cimm.1996.0060.
Mammary tumor viruses (MMTVs) as well as their endogenous counterparts encode superantigens which react with T cells expressing particular T cell receptor V beta chains. Several lines of evidence indicated that MHC class II is required for the functional presentation of these superantigens. Here we provide direct proof that the function of superantigens is abrogated in the absence of MHC class II expression. No deletion of Mls-1-reactive T cells was observed in MHC class II-deficient mice, and splenocytes from these animals did not stimulate Mls-1-reactive T cell hybrids in vitro. Furthermore, the viral spread in MHC class II-deficient mice, maternally infected with MMTV(C3H), was severely reduced. While initial infection in the gut-associated lymphocytes was comparable between MHC class II-deficient and normal mice, the level of infection in the spleen and the mammary tissue was much lower in the deficient animals. Quantitation of proviral DNA in spleen revealed a direct correlation between the magnitude of superantigen stimulation and degree of infection. These experiments document the direct effect of superantigen stimulation on viral amplification.
乳腺肿瘤病毒（MMTVs）及其内源性对应物编码与表达特定T细胞受体Vβ链的T细胞发生反应的超抗原。多项证据表明，这些超抗原的功能性呈递需要MHC II类分子。在此我们提供直接证据，证明在缺乏MHC II类分子表达的情况下超抗原的功能丧失。在MHC II类缺陷小鼠中未观察到Mls-1反应性T细胞的缺失，并且这些动物的脾细胞在体外不能刺激Mls-1反应性T细胞杂交瘤。此外，在经MMTV（C3H）母体感染的MHC II类缺陷小鼠中，病毒传播严重减少。虽然在MHC II类缺陷小鼠和正常小鼠中，肠道相关淋巴细胞的初始感染情况相当，但缺陷动物脾脏和乳腺组织中的感染水平要低得多。脾脏中前病毒DNA的定量分析揭示了超抗原刺激强度与感染程度之间的直接相关性。这些实验证明了超抗原刺激对病毒扩增的直接影响。
