重组γ干扰素对I类主要组织相容性抗原H-2K和H-2D的差异诱导。白血病病毒诱导的肿瘤中Kk增强缺失是由于顺式显性效应。
Differential induction of H-2K versus H-2D class I major histocompatibility antigens by recombinant gamma interferon. Lack of Kk augmentation in a leukemia virus-induced tumor is due to a cis-dominant effect.
作者信息
Green W R, Rich R F, Beadling C
机构信息
Department of Microbiology, Dartmouth Medical School, Hanover, New Hampshire 03756.
出版信息
J Exp Med. 1988 May 1;167(5):1616-24. doi: 10.1084/jem.167.5.1616.
Abstract
T-T tumor hybrids were constructed between the AKR SL3 thymoma and an H-2-distinguishable thymoma cell line. Hybrids were stimulated with IFN-gamma to determine whether the differential augmentation of H-2D vs. H-2K class I antigen expression by AKR SL3 in response to IFN-gamma was due to effects cis or trans to the noninducible Kk gene. For each of a large number of hybrids tested, the expression of H-2Db, Kb, and Dk, but not Kk, was substantially enhanced by murine rIFN-gamma. These results suggested that the lack of induction of the Kk gene was due to an alteration cis to Kk rather than to the presence or absence of K region-specific, trans-acting negative or positive factors, respectively.
摘要
在AKR SL3胸腺瘤和一种H-2可区分的胸腺瘤细胞系之间构建了T-T肿瘤杂交细胞。用γ干扰素刺激杂交细胞，以确定AKR SL3对γ干扰素反应时H-2D与H-2K I类抗原表达的差异增强是由于对非诱导性Kk基因的顺式作用还是反式作用。对于大量测试的杂交细胞中的每一个，小鼠重组γ干扰素可显著增强H-2Db、Kb和Dk的表达，但不增强Kk的表达。这些结果表明，Kk基因缺乏诱导是由于Kk顺式改变，而不是分别由于K区域特异性反式作用的负性或正性因子的存在或缺失。
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