Golovkina T V, Chervonsky A, Prescott J A, Janeway C A, Ross S R
Department of Biochemistry, University of Illinois College of Medicine, Chicago 60612.
J Exp Med. 1994 Feb 1;179(2):439-46. doi: 10.1084/jem.179.2.439.
Transgenic mice expressing either the mouse mammary tumor virus (MMTV) superantigen gene (sag) alone or in combination with the viral envelope genes (env) (LEL), or all of the viral genes (gag, pol, env, and sag) (HYB PRO), deleted V beta 14+ T cells from their immune repertoire. However, only LEL or HYB PRO transgenic antigen-presenting cells were capable of stimulating a proliferative response from nontransgenic primary T cells or interleukin 2 production from a V beta 15-bearing T cell hybridoma. These T cell responses could be inhibited by a monospecific antibody directed against the MMTV gp52 cell surface glycoprotein. These results indicate that the MMTV gp52 gene product participates in the presentation of superantigen to T cells, resulting in their stimulation, a requisite step in the MMTV infection pathway. Thus, gp52 could play a role in the transfer of virus between different subsets of lymphocytes.
表达单独的小鼠乳腺肿瘤病毒(MMTV)超抗原基因(sag)或与病毒包膜基因(env)(LEL)组合,或所有病毒基因(gag、pol、env和sag)(HYB PRO)的转基因小鼠,其免疫库中缺失了Vβ14 + T细胞。然而,只有LEL或HYB PRO转基因抗原呈递细胞能够刺激非转基因原代T细胞的增殖反应或来自携带Vβ15的T细胞杂交瘤产生白细胞介素2。这些T细胞反应可被针对MMTV gp52细胞表面糖蛋白的单特异性抗体抑制。这些结果表明,MMTV gp52基因产物参与超抗原向T细胞的呈递,导致T细胞受到刺激,这是MMTV感染途径中的一个必要步骤。因此,gp52可能在病毒在淋巴细胞不同亚群之间的转移中发挥作用。