Major and minor Kb-restricted epitopes encoded by the endogenous ecotropic murine leukemia virus AKR623 that are recognized by anti-AKR/Gross MuLV CTL.
Major and minor Kb-restricted epitopes encoded by the endogenous ecotropic murine leukemia virus AKR623 that are recognized by anti-AKR/Gross MuLV CTL.
复制标题
由内源性亲嗜性鼠白血病病毒 AKR623 编码的主要和次要 Kb 限制性表位，可被抗 AKR/Gross MuLV CTL 识别。
DOI：
10.1089/vim.1994.7.51
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发表时间：
1994
期刊：
影响因子：
2.2
通讯作者：
Green,WR
中科院分区：
文献类型：
--
作者：
White,HD;Roeder,DA;Lam,T;Green,WR
C57BL/6小鼠可对组织相容性AKR/粗鼠白血病病毒（MuLV）细胞表面抗原阳性（GCSA+）肿瘤细胞产生类型特异性和I类h - 2kb限制性CTL反应。已知这些抗akr /Gross MuLV CTL也能裂解表达MuLV分子克隆AKR623（源自内源性生态性MuLV前病毒emv-11）的SC.Kb/623靶细胞。为了帮助鉴定这些CTL识别的AKR623病毒表位，用两个亲本质粒pAKR623和pAK7构建了四个嵌合原病毒。研究表明，表达emv-14衍生分子克隆AK7的SC.Kb/7成纤维细胞靶标仅被抗akr /Gross MuLV CTL较差地裂解。利用嵌合体感染的SC.Kbcells作为抗akr /Gross MuLV CTL的靶标的实验数据支持了先前鉴定的位于病毒p15E跨膜包膜蛋白肽TM134-141 （KSP-WFTTL）内的免疫优势表位的位置。此外，利用kb基序定义的AKR623编码肽和使用嵌合病毒获得的数据，可以鉴定出另外三个抗akr /Gross MuLV CTL表位。代表这些表位的肽，MA125-132 (RSALYPAL), RT142-149 （SHRWYTVL）和RT456-463 (RMTHYQAM)，在这里被表征为它们在体外对EMV靶细胞进行裂解和刺激肿瘤引发的脾细胞的能力。这些额外表位的鉴定和表征可以更好地理解针对GCSA+肿瘤细胞的CTL反应和针对EMV-14和AK7的功能失调CTL反应。
C57BL/6 mice can generate a type-specific and class I H-2Kb-restricted CTL response against histocompatible AKR/Gross murine leukemia virus (MuLV) cell surface antigen positive (GCSA+) tumor cells. These anti-AKR/Gross MuLV CTL are also known to lyse SC.Kb/623 target cells expressing the molecular MuLV clone AKR623 (derived from the endogenous ecotropic MuLV provirusemv-11). To help identify AKR623 viral epitopes recognized by these CTL, four chimeric proviruses were constructed from two parental plasmids, pAKR623 and pAK7. It has been shown that SC.Kb/7 fibroblast targets expressing theemv-14-derived molecular clone AK7 are only poorly lysed by anti-AKR/Gross MuLV CTL. Data from experiments employing SC.Kbcells infected with the chimeras as targets against anti-AKR/Gross MuLV CTL supported the location of a previously identified immunodominant epitope located within the viral p15E transmembrane envelope protein, peptide TM134-141 (KSP-WFTTL). Furthermore, the use of Kb-motif-defined AKR623 encoded peptides together with data obtained using the chimeric viruses allowed the identification of three additional anti-AKR/Gross MuLV CTL epitopes. Peptides representing these epitopes, MA125-132 (RSALYPAL), RT142-149 (SHRWYTVL), and RT456-463 (RMTHYQAM), are characterized herein with respect to their ability to confer lysis upon EMV− target cells and to stimulate tumor primed splenocytesin vitro. The identification and characterization of these additional epitopes allow for a better understanding of both the CTL response against GCSA+tumor cells and the dysfunctional CTL response against EMV-14 and AK7.