Held W, Waanders G A, MacDonald H R, Acha-Orbea H
Ludwig Institute for Cancer Research, Lausanne Branch, Epalinges, Switzerland.
Int Immunol. 1994 Sep;6(9):1403-7. doi: 10.1093/intimm/6.9.1403.
Superantigens (SAgs) encoded by infectious mouse mammary tumor viruses (MMTVs) play a crucial role in the viral life cycle. Their expression by infected B cells induces a proliferative immune response by SAg-reactive T cells which amplifies MMTV infection. This response most likely ensures stable MMTV infection and transmission to the mammary gland. Since T cell reactivity to SAgs from endogenous Mtv loci depends on MHC class II molecules expressed by B cells, we have determined the ability of MMTV to infect various MHC congenic mice. We show that MHC class II I-E+ compared with I-E- mouse strains show higher levels of MMTV infection, most likely due to their ability to induce a vigorous SAg-dependent immune response following MMTV encounter. Inefficient infection is observed in MHC class II I-E- mice, which have been shown to present endogenous SAgs poorly. Therefore, during MMTV infection the differential ability of MHC class II molecules to form a functional complex with SAg determines the magnitude of the proliferative response of SAg-reactive T cells. This in turn influences the degree of T cell help provided to infected B cells and therefore the efficiency of amplification of MMTV infection.
由感染性小鼠乳腺肿瘤病毒（MMTVs）编码的超抗原（SAgs）在病毒生命周期中起着关键作用。被感染的B细胞表达这些超抗原会诱导超抗原反应性T细胞产生增殖性免疫反应，从而放大MMTV感染。这种反应很可能确保了MMTV的稳定感染以及向乳腺的传播。由于T细胞对内源Mtv基因座超抗原的反应性取决于B细胞表达的MHC II类分子，我们已经确定了MMTV感染各种MHC同基因小鼠的能力。我们发现，与I-E-小鼠品系相比，MHC II类I-E+小鼠品系表现出更高水平的MMTV感染，这很可能是因为它们在接触MMTV后能够诱导强烈的超抗原依赖性免疫反应。在MHC II类I-E-小鼠中观察到感染效率低下，这些小鼠已被证明呈递内源性超抗原的能力较差。因此，在MMTV感染期间，MHC II类分子与超抗原形成功能复合物的差异能力决定了超抗原反应性T细胞增殖反应的强度。这反过来又影响了为被感染B细胞提供的T细胞辅助程度，进而影响了MMTV感染的放大效率。
