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在AKR.H-2b和AKR.H-2b:Fv-1b小鼠品系中诱导抗小鼠白血病病毒细胞毒性T淋巴细胞

Induction of anti-MuLV cytotoxic T lymphocytes in the AKR.H-2b and AKR.H-2b:Fv-1b mouse strains.

作者信息

Wegmann K W, Blank K J, Green W R

机构信息

Department of Microbiology, Dartmouth Medical School, Hanover, New Hampshire 03756.

出版信息

Cell Immunol. 1988 May;113(2):308-19. doi: 10.1016/0008-8749(88)90029-9.

Abstract

Following secondary in vitro sensitization with AKR/Gross virus-induced tumors, AKR.H-2b:Fv-1b mice develop cytotoxic T lymphocytes (CTL) specific for AKR/Gross viral antigens. It has recently been determined that the responder status of AKR.H-2b:Fv-1b to AKR/Gross virus declines with age. The nonresponsiveness observed in AKR.H-2b:Fv-1b is similar to that observed in AKR.H-2b mice which (regardless of age) does not develop anti-AKR/Gross virus CTL. It was of interest to determine the ability of these congenic mouse strains to respond to other murine leukemia viruses (MuLV). This was accomplished by immunizing AKR.H-2b and young or moderately aged AKR.H-2b:Fv-1b with Friend-Moloney-Rauscher (FMR) virus-induced tumors, and assessing the ability of anti-FMR CTL to develop following secondary in vitro stimulation. It was observed that both AKR.H-2b and AKR.H-2b:Fv-1b developed specific anti-FMR virus CTL. Similarly, following tumor challenge AKR.H-2b mice were unable to prevent the outgrowth of a syngeneic AKR/Gross virus-induced tumor, but were able to reject a syngeneic FMR virus-induced tumor.

摘要

用AKR/Gross病毒诱导的肿瘤进行二次体外致敏后,AKR.H-2b:Fv-1b小鼠产生了针对AKR/Gross病毒抗原的细胞毒性T淋巴细胞(CTL)。最近已确定,AKR.H-2b:Fv-1b对AKR/Gross病毒的反应状态会随着年龄的增长而下降。在AKR.H-2b:Fv-1b中观察到的无反应性与在AKR.H-2b小鼠中观察到的情况相似,后者(无论年龄大小)都不会产生抗AKR/Gross病毒CTL。确定这些同源小鼠品系对其他鼠白血病病毒(MuLV)的反应能力很有意义。这是通过用Friend-Moloney-Rauscher(FMR)病毒诱导的肿瘤免疫AKR.H-2b以及年轻或中年的AKR.H-2b:Fv-1b,并评估二次体外刺激后抗FMR CTL的产生能力来实现的。观察到AKR.H-2b和AKR.H-2b:Fv-1b都产生了特异性抗FMR病毒CTL。同样,在肿瘤攻击后,AKR.H-2b小鼠无法阻止同基因AKR/Gross病毒诱导的肿瘤生长,但能够排斥同基因FMR病毒诱导的肿瘤。

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