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Locus-specific de novo methylation down-regulates MHC class I in S49 lymphomas.

作者信息

Rubocki R J, Berrigan B E, Speaks S L, Wisecarver J L

机构信息

University of Nebraska Medical Center, Dept. of Pathology and Microbiology, Omaha 68198, USA.

出版信息

Immunogenetics. 1996;43(1-2):63-7. doi: 10.1007/BF00186605.

DOI:10.1007/BF00186605
PMID:8537124
Abstract
摘要

相似文献

1
Locus-specific de novo methylation down-regulates MHC class I in S49 lymphomas.位点特异性从头甲基化下调S49淋巴瘤中的主要组织相容性复合体I类分子。
Immunogenetics. 1996;43(1-2):63-7. doi: 10.1007/BF00186605.
2
Locus-specific regulation of Kd, Dd, and Ld class I genes in the BALB/c S49 lymphoma sublines.BALB/c S49淋巴瘤亚系中Kd、Dd和Ld I类基因的位点特异性调控。
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3
Expression of hemopoietic histocompatibility antigens on H-2-loss variants of F1 hybrid lymphoma cells: evidence consistent with trans gene regulation.造血组织相容性抗原在F1杂交淋巴瘤细胞的H-2缺失变异体上的表达：与转基因调控一致的证据。
J Immunol. 1987 Apr 15;138(8):2734-8.
4
Cis-acting elements determine the locus-specific shutoff of class I major histocompatibility genes in murine S49 lymphoma sublines.顺式作用元件决定了小鼠S49淋巴瘤亚系中I类主要组织相容性基因的位点特异性关闭。
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5
Differential lack of class I H-2d antigen expression by sublines of the BALB/c S49 T cell lymphoma.BALB/c S49 T细胞淋巴瘤亚系中I类H-2d抗原表达的差异缺失
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6
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Exp Clin Immunogenet. 1986;3(2):98-110.
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H-2 class I gene analysis in 3-methylcholanthrene-induced murine fibrosarcomas.3-甲基胆蒽诱导的小鼠纤维肉瘤中的H-2 I类基因分析
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MHC class I antigen expression and alterations induced by rIFN gamma in tumor hybrid cell immunogenicity.MHC I类抗原表达及重组干扰素γ诱导的改变对肿瘤杂交细胞免疫原性的影响
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Expression of TL, H-2, and chimeric H-2/TL genes in transgenic mice: abnormal thymic differentiation and T-cell lymphomas in a TL transgenic strain.TL、H-2和嵌合H-2/TL基因在转基因小鼠中的表达：TL转基因品系中的胸腺分化异常和T细胞淋巴瘤
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Immunisation with modified HPV16 E7 genes against mouse oncogenic TC-1 cell sublines with downregulated expression of MHC class I molecules.用修饰的人乳头瘤病毒16型E7基因对主要组织相容性复合体I类分子表达下调的小鼠致癌TC-1细胞亚系进行免疫接种。
Vaccine. 2003 Mar 7;21(11-12):1125-36. doi: 10.1016/s0264-410x(02)00519-4.

本文引用的文献

1
Interferon, β-2-microglobulin and immunoselection in the pathway to malignancy A blinkered view from Nag's Head Yard.恶性肿瘤发生途径中的干扰素、β2微球蛋白与免疫选择：来自纳格斯海德场院的片面观点
Immunol Today. 1983 Aug;4(8):211-3. doi: 10.1016/0167-5699(83)90027-0.
2
Identification of human cancers deficient in antigen processing.缺乏抗原加工的人类癌症的鉴定。
J Exp Med. 1993 Feb 1;177(2):265-72. doi: 10.1084/jem.177.2.265.
3
Tumor-specific lysis of human renal cell carcinomas by tumor-infiltrating lymphocytes. I. HLA-A2-restricted recognition of autologous and allogeneic tumor lines.
肿瘤浸润淋巴细胞对人肾细胞癌的肿瘤特异性裂解。I. HLA-A2 限制的自体和同种异体肿瘤细胞系识别
J Immunol. 1993 Oct 15;151(8):4209-20.
4
Tumor escape from immune response by variation in HLA expression and other mechanisms.肿瘤通过HLA表达的变化及其他机制逃避免疫反应。
Ann N Y Acad Sci. 1993 Aug 12;690:42-9. doi: 10.1111/j.1749-6632.1993.tb43994.x.
5
Rejection of K1735 murine melanoma in syngeneic hosts requires expression of MHC class I antigens and either class II antigens or IL-2.同基因宿主中K1735鼠黑色素瘤的排斥反应需要MHC I类抗原以及II类抗原或白细胞介素-2的表达。
J Immunol. 1993 Jul 1;151(1):244-55.
6
Loss of transporter protein, encoded by the TAP-1 gene, is highly correlated with loss of HLA expression in cervical carcinomas.由TAP-1基因编码的转运蛋白缺失与宫颈癌中HLA表达缺失高度相关。
J Exp Med. 1994 Jan 1;179(1):335-40. doi: 10.1084/jem.179.1.335.
7
MHC antigen expression by melanomas recovered from mice treated with allogeneic mouse fibroblasts genetically modified for interleukin-2 secretion and the expression of melanoma-associated antigens.从用经基因改造可分泌白细胞介素-2并表达黑色素瘤相关抗原的同种异体小鼠成纤维细胞处理的小鼠中回收的黑色素瘤的MHC抗原表达。
Cancer Immunol Immunother. 1994 Mar;38(3):185-93. doi: 10.1007/BF01525640.
8
In vivo priming of two distinct antitumor effector populations: the role of MHC class I expression.两种不同抗肿瘤效应细胞群的体内启动：MHC I类分子表达的作用
J Exp Med. 1994 Apr 1;179(4):1215-24. doi: 10.1084/jem.179.4.1215.
9
Rejection of transplantable AKR leukaemia cells following MHC DNA-mediated cell transformation.MHC DNA介导的细胞转化后对可移植AKR白血病细胞的排斥反应。
Nature. 1984;311(5988):750-2. doi: 10.1038/311750a0.
10
DNAase I-hypersensitive sites of chromatin.染色质的脱氧核糖核酸酶I超敏位点
Cell. 1981 Dec;27(3 Pt 2):413-5. doi: 10.1016/0092-8674(81)90381-0.