LEUKEMIA-ASSOCIATED TRANSPLANTATION ANTIGENS RELATED TO MURINE LEUKEMIA VIRUS
LEUKEMIA-ASSOCIATED TRANSPLANTATION ANTIGENS RELATED TO MURINE LEUKEMIA VIRUS
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与鼠白血病病毒相关的白血病相关移植抗原
DOI：
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发表时间：
1973
影响因子：
15.3
通讯作者：
L. Old
中科院分区：
文献类型：
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作者：
H. Sato;E. A. Boyse;T. Aoki;C. Iritani;L. Old
两种BALB放射性白血病被BALB与某些其他小鼠品系的杂交种强烈排斥，尽管BALB小鼠本身没有表现出任何可检测的抵抗力。用逐渐增加的接种物免疫的杂交种对200 × 106或更多的白血病细胞具有抗性;它们的血清在体外对白血病细胞具有细胞毒性，并保护BALB小鼠免受这些BALB白血病的攻击。由此鉴定的抗原系统被命名为X.1。在（BALB × B6）杂交后代中，抗性的主要决定因素是H-2 K区的B6基因。这可能是礼来公司的Rgv-1（对粗大病毒的抗性）基因座，因此在这种情况下可以将其鉴定为Ir（免疫应答）等位基因，该等位基因赋予对MuLV和白血病细胞上的X.1抗原的应答能力，因此负责杂交小鼠产生X.1抗体和排斥X.1+白血病细胞。用X.1抗血清（来自免疫的杂交种）进行的免疫电子显微镜检查显示，白血病细胞产生的细胞表面和病毒体上都有标记。X.1是仅包含一种抗原还是包含一种以上抗原尚不清楚。3例辐射诱导的BALB白血病、1例A株辐射诱导的白血病和15/15例AKR原发性自发性白血病经细胞毒性试验分型为X.1+。其他几种白血病，包括一种由A代Gross病毒诱导的白血病和一种在（B6 x AKR）F1杂交种中携带的长移植AKR腹水白血病，均为X.1-。白血病发病率高的品系的正常小鼠和另一品系（129）表达X.1抗原，但显然数量太少，无法在体外进行某些检测;然而，通过体内吸收方法，这些品系可分型为X.1+，而其他品系为X.1-。我们暂时将X.1抗原系统归因于MuLV的一种亚型，该亚型不是A代Gross病毒，并且可能不是白血病发病率高的菌株中的主要亚型。在杂交体中反复传代后，其中一种BALB白血病对杂交体的排斥反应具有相对抗性，部分丧失了对体外X.1抗血清的敏感性，并且在电子显微镜下观察到产生较少的病毒粒子。未处理的BALB × B6杂交小鼠血清中常含有抗白血病细胞的细胞毒抗体，其中有些可能是抗X细胞的。但另一种常见的抗体，对C57 BL白血病EL 4具有细胞毒性，似乎属于另一个（未定义）系统。
Two BALB radiation leukemias are strongly rejected by hybrids of BALB with certain other mouse strains, although BALB mice themselves exhibit no detectable resistance whatever. Hybrids immunized with progressively increased inocula are resistant to 200 x 106 or more leukemia cells; their serum is cytotoxic for the leukemia cells in vitro and protects BALB mice against challenge with these BALB leukemias. The antigenic system thus identified has been named X.1. In (BALB x B6) hybrids the major determinant of resistance was shown to be a B6 gene in the K region of H-2. This is likely to be the Rgv-1 (Resistance to gross virus) locus of Lilly, which may thus be identified in this case as an Ir (Immune response) allele conferring ability to respond to X.1 antigen on MuLV and leukemia cells, and so responsible for production of X.1 antibody and the rejection of X.1+ leukemia cells by hybrid mice. Immunoelectron microscopy with X.1 antiserum (from immunized hybrids) shows labeling both on the cell surface and on virions produced by the leukemia cells. It is not known whether X.1 comprises only one or more than one antigen. Three radiation-induced BALB leukemias, one A strain radiation-induced leukemia, and 15/15 AKR primary spontaneous leukemias were typed X.1+ by the cytotoxicity test. Several other leukemias, including one induced by passage A Gross virus and one long-transplanted AKR ascites leukemia carried in (B6 x AKR)F1 hybrids, were X.1-. Normal mice of strains with a high incidence of leukemia and one other strain (129) express X.1 antigen, but evidently in amounts too small for certain detection in vitro; by the method of absorption in vivo, however, these strains could be typed X.1+ and other strains X.1-. We ascribe the X.1 antigen system tentatively to a sub-type of MuLV that is not passage A Gross virus and is probably not the dominant sub-type in strains with a high incidence of leukemia. After repeated passage in hybrids, one of the BALB leukemias became relatively resistant to rejection by the hybrid, partially lost its sensitivity to X.1 antiserum in vitro, and in electron micrographs was seen to produce fewer virions. The serum of untreated (BALB x B6) hybrids often contains cytotoxic antibody against leukemia cells, some of it probably anti-X.1. But another commonly occurring antibody, which is cytotoxic for C57BL leukemia EL4, appears to belong to another (undefined) system.