Gene analysis of human parainfluenza virus type 4 and analysis of virus receptor

我们分析了人副流感病毒4型L蛋白的基因序列。CD98是一种广泛表达的125 kDa的细胞表面异质性蛋白。在有丝分裂原、超抗原、常规抗原以及佛波酯(PMA)和离子霉素联合诱导的淋巴细胞活化过程中，其表达上调。然而，CD98在免疫系统中的作用还不是很清楚。探讨CD98在淋巴细胞增殖中的作用，特别是与IL-2/IL-2R系统的相关性。抗小鼠CD98重链(MCD98HC)的单抗(MAb)(26-24)可抑制ConA刺激的淋巴细胞增殖。然而，抗CD98HC单抗(26-24)不能抑制Coil A刺激的淋巴细胞产生IL-2，此外，重组IL-2可诱导亚最佳剂量ConA刺激的淋巴细胞合成大量DNA，但不能诱导淋巴细胞表达CD98HC。抗CD98HC单抗不能抑制IL-2Rα的表达。抑制α合成的抗IL-2R单抗不能抑制CD98HC的表达。综上所述，CD98系统在淋巴细胞活化中独立于IL-2-IL-2R系统。

We analyzed the gene sequence of human parainfluenza virus type 4 L protein. More than 80% was finished, and only gene ending region was remaining.CD98 is a widely expressed cell surface heterodimetric protein of 125kDa. Its expression is up-regulated during lymphocyte activation induced by mitogen, superantigen, conventional antigen, arid a combination of phorbol myristate acstate (PMA) and ionomycin. However, the role of CD98 in the immune system is not so well understood. The role of CD98 in lymphocyte proliferation was investigated, especially in correlation with IL-2/IL-2R system. Monoclonal antibody (mAb) (26-24) directed against murine CD98 heavy chain (mCD98HC) suppressed the proliferation of lymphocytes stimulated with concunavalin A (Con A). However, anti-CD98HC mAb (26-24) did not inhibit the production of interleukin 2 (IL-2) by lymphocyte stimulated with Coil A. In addition, IL-2 (recombinant), which induced considerable DNA synthesis of lymphocytes stimulated with sub-optimal dose of Con A, did not induce CD98HC expression in lymphocytes. Anti-mCD98HC mAb did not suress the expression of IL-2Rα. Anti-LL-2RαmAb, which suppressed DNA synthesis, did not inhibit the expression of CD98HC. Taken together with these findings, it was inferred that CD98 system is independent of IL-2-IL-2R system in lymphocyte activation.