Rudy C K, Kraus E, Palmer E, Huber B T
Department of Pathology, Tufts University School of Medicine, Boston, Massachusetts 02111.
J Exp Med. 1992 Jun 1;175(6):1613-21. doi: 10.1084/jem.175.6.1613.
Mls-1 is an endogenous superantigen that leads to in vivo deletion and in vitro stimulation of T cell receptor (TCR) V beta 6-, 7-, 8.1-, and 9-expressing cells. The MA/MyJ mouse deletes the identical set of TCR from its mature T cell repertoire; however, it does not contain Mtv-7, the murine mammary tumor provirus (MMTV), whose sag gene encodes Mls-1. Interestingly, the superantigen activity of this mouse strain segregates with a new mammary tumor provirus, Mtv-43, not seen in other inbred strains. The predicted amino acid sequence of the sag gene of Mtv-43 was compared with that of Mtv-7. Strikingly, the COOH terminus of the two molecules is very similar, while all other MMTV-encoded superantigens differ 100% in this segment.
Mls-1是一种内源性超抗原，可导致体内表达T细胞受体（TCR）Vβ6、7、8.1和9的细胞缺失，并在体外刺激这些细胞。MA/MyJ小鼠从其成熟T细胞库中删除了相同的TCR集合；然而，它不包含Mtv-7，即鼠乳腺肿瘤前病毒（MMTV），其sag基因编码Mls-1。有趣的是，该小鼠品系的超抗原活性与一种新的乳腺肿瘤前病毒Mtv-43相关，这在其他近交系中未见。将Mtv-43的sag基因预测氨基酸序列与Mtv-7的进行了比较。令人惊讶的是，这两个分子的COOH末端非常相似，而所有其他MMTV编码的超抗原在该片段中100%不同。
