THE IMMUNE-RESPONSE OF THE MOUSE TO LYMPHOCYTIC CHORIOMENINGITIS VIRUS .5. HIGH NUMBERS OF CYTOLYTIC LYMPHOCYTES-T ARE GENERATED IN THE SPLEEN DURING ACUTE INFECTION
THE IMMUNE-RESPONSE OF THE MOUSE TO LYMPHOCYTIC CHORIOMENINGITIS VIRUS .5. HIGH NUMBERS OF CYTOLYTIC LYMPHOCYTES-T ARE GENERATED IN THE SPLEEN DURING ACUTE INFECTION
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DOI：
10.1002/eji.1830170707
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发表时间：
1987-07-01
影响因子：
5.4
通讯作者：
LEHMANNGRUBE, F
中科院分区：
文献类型：
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作者：
MOSKOPHIDIS, D;ASSMANNWISCHER, U;LEHMANNGRUBE, F
在淋巴细胞性脉络膜脑膜炎（LCM）病毒急性感染的C57BL/6J（B6）和CBA/J（CBA）小鼠的脾脏中，采用有限稀释法计数能够在体外发育成LCM病毒特异性溶细胞克隆的淋巴细胞。病毒接种后每隔一段时间，在微量培养板的多个孔中用病毒感染的同源刺激细胞和T细胞生长因子培养规定数量的细胞。 7 天后，测试单个细胞培养物引起受感染和未受感染的同基因靶细胞释放 51Cr 的能力。在接种来自未感染小鼠或三天前感染小鼠的脾细胞的培养物中，没有观察到细胞溶解活性。第5天，检测到细胞发育成LCM病毒特异性溶细胞效应细胞。它们的数量增加，在感染后第 8 至 9 天，B6 和 CBA 小鼠的数值分别约为 1/10 和 1/200。低比例的微培养物被证明对未感染的同基因靶细胞也具有溶细胞作用，但由此释放的计数始终远低于从受感染的靶细胞中释放的计数，并且种子细胞和阳性培养物之间不存在规则的剂量反应关系。通过阴性和阳性选择程序测定应答细胞的细胞表面抗原表明它们主要是T淋巴细胞并且表达Lyt-2但不表达L3T4表面标记。大多数LCM病毒特异性克隆的裂解受到主要组织相容性基因复合体（MHC）产物的限制，但也有少数裂解，此外，同种异体感染或未感染的靶标；然而，没有观察到一致的同种异体反应性模式。此外，一部分培养物的细胞也裂解未感染的YAC细胞。这种自然杀伤样活性可能是 T 淋巴细胞在长期培养过程中获得的。我们得出的结论是，在 LCM 病毒急性感染期间获得体外发育成 LCM 病毒特异性溶细胞克隆的能力的大多数脾细胞源自 MHC 限制性 Lyt-2+、L3T4- 抗原特异性溶细胞 T 淋巴细胞及其活化前体。
In the spleens of C57BL/6J (B6) and CBA/J (CBA) mice undergoing acute infection with lymphocytic choriomeningitis (LCM) virus, lymphocytes with the ability to develop in vitro into LCM virus-specific cytolytic clones were enumerated by use of the limiting dilution method. At intervals after virus inoculation, defined numbers of cells were cultivated with virus-infected syngeneic stimulator cells and T cell growth factor in multiple wells of microculture plates. After 7 days, individual cell cultures were tested for their ability to cause release of 51Cr from infected and uninfected syngeneic target cells. In cultures seeded with spleen cells from uninfected mice or from mice infected 3 days previously, no cytolytic activity was observed. On day 5, cells developing into LCM virus-specific cytolytic effector cells were detected. They rose in numbers, and on days 8 to 9 after infection, values of approximately 1/10 and 1/200 in B6 and CBA mice, respectively, were calculated. A low proportion of microcultures proved cytolytic also for noninfected syngeneic target cells, but the counts thus released were consistently much lower than the counts set free from infected targets, and no regular dose-response relationships existed between seeded cells and positive cultures. Determination of cell surface antigens of responder cellsby negative and positive selection procedures disclosed that they were predominantly T lymphocytes and expressed Lyt-2 but not L3T4 surface markers. Lysis by the great majority of LCM virus-specific clones was restricted by products of the major histocompatibility gene complex (MHC), but a few lysed, in addition, allogeneic infected or uninfected targets; however, a consistent pattern of alloreactivity was not observed. Furthermore, cells of a proportion of the cultures also lysed uninfected YAC cells. Probably this natural killer-like activity was acquired by T lymphocytes during prolonged cultivation. We concluded that most spleen cells that during acute infection with LCM virus attained the ability to develop in vitro into LCM virus-specific cytolytic clones were derived from MHC-restricted Lyt-2+, L3T4- antigenic-specific cytolytic T lymphocytes and their activated precursors.