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A new gene encoding the ligand for deletion of T cells bearing Tcrb-V6 and V8.1 (Mtv-50).

作者信息

Niimi N, Wajjwalku W, Ando Y, Tomida S, Ueda M, Yoshikai Y

机构信息

Department of Oral Surgery, Nagoya University School of Medicine, Japan.

出版信息

Immunogenetics. 1994;40(4):312. doi: 10.1007/BF00189982.

DOI:10.1007/BF00189982
PMID:8082898
Abstract
摘要

相似文献

1
A new gene encoding the ligand for deletion of T cells bearing Tcrb-V6 and V8.1 (Mtv-50).
Immunogenetics. 1994;40(4):312. doi: 10.1007/BF00189982.
2
Identification of two V beta 7-specific viral superantigens.两种Vβ7特异性病毒超抗原的鉴定。
J Immunol. 1994 Jan 1;152(1):65-71.
3
Co-segregation of a gene encoding a deletion ligand for Tcrb-V3+ T cells with Mtv-3.
Immunogenetics. 1991;34(4):227-30. doi: 10.1007/BF00215257.
4
Thymic repertoire selection by superantigens: presentation by human and mouse MHC molecules.超抗原对胸腺库的选择：人源和鼠源MHC分子的呈递
Thymus. 1994;23(1):1-13.
5
Delay in expression of a mammary tumor provirus is responsible for defective clonal deletion during postnatal period.乳腺肿瘤前病毒表达的延迟是出生后时期克隆清除缺陷的原因。
Eur J Immunol. 1994 Feb;24(2):488-91. doi: 10.1002/eji.1830240235.
6
Expression of Mtv-7 sag gene in vivo using a retroviral vector results in selective inactivation of superantigen reactive T cells.使用逆转录病毒载体在体内表达Mtv-7 sag基因会导致超抗原反应性T细胞的选择性失活。
J Immunol. 1994 Feb 1;152(3):1039-46.
7
Mls superantigens: how retroviruses influence the expressed T cell receptor repertoire.Mls超抗原：逆转录病毒如何影响表达的T细胞受体库。
Semin Immunol. 1992 Oct;4(5):313-8.
8
Mouse endogenous superantigens: Ms and Mls-like determinants encoded by mouse retroviruses.
Curr Protoc Immunol. 2001 May;Appendix 1:Appendix 1F. doi: 10.1002/0471142735.ima01fs17.
9
Tcrb-V3+ T-cell deletion and a mouse mammary tumor provirus, Mtv-27.Tcrb-V3+ T细胞缺失与一种小鼠乳腺肿瘤前病毒Mtv-27
Immunogenetics. 1992;36(5):302-5. doi: 10.1007/BF00215658.
10
Alleles of highly homologous rat T cell receptor beta-chain variable segments 8.2 and 8.4: strain-specific expression, reactivity to superantigens, and binding of the mAb R78.高度同源的大鼠T细胞受体β链可变区8.2和8.4的等位基因：品系特异性表达、对超抗原的反应性以及单克隆抗体R78的结合
J Immunol. 1996 Nov 15;157(10):4436-41.

引用本文的文献

1
Expression of mouse mammary tumor virus superantigen accelerates tumorigenicity of myeloma cells.小鼠乳腺肿瘤病毒超抗原的表达加速骨髓瘤细胞的致瘤性。
J Virol. 2000 Sep;74(18):8226-33. doi: 10.1128/jvi.74.18.8226-8233.2000.
2
Superantigens related to B cell hyperplasia.与B细胞增生相关的超抗原。
Springer Semin Immunopathol. 1996;17(4):285-306. doi: 10.1007/BF01795130.

本文引用的文献

1
A gene encoding the ligand for deletion of T cells bearing TcrV beta 6 and V beta 8.1 cosegregates with a new endogenous mouse mammary tumor virus.一个编码能使携带TcrVβ6和Vβ8.1的T细胞缺失的配体的基因，与一种新的内源性小鼠乳腺肿瘤病毒共分离。
Immunogenetics. 1993;37(5):397-400. doi: 10.1007/BF00216807.
2
The mouse mammary tumor virus envelope gene product is required for superantigen presentation to T cells.小鼠乳腺肿瘤病毒包膜基因产物是超抗原呈递给T细胞所必需的。
J Exp Med. 1994 Feb 1;179(2):439-46. doi: 10.1084/jem.179.2.439.
3
New superantigen specificity created by two amino acid replacements.
由两个氨基酸替换产生的新的超抗原特异性。
Immunogenetics. 1993;38(5):367-9. doi: 10.1007/BF00210480.
4
T-cell receptor V beta use predicts reactivity and tolerance to Mlsa-encoded antigens.T细胞受体Vβ的使用可预测对Mlsa编码抗原的反应性和耐受性。
Nature. 1988 Mar 3;332(6159):40-5. doi: 10.1038/332040a0.
5
Mls and tolerance.Mls与耐受性
Immunol Rev. 1989 Feb;107:29-59. doi: 10.1111/j.1600-065x.1989.tb00002.x.
6
A third T-cell receptor beta-chain variable region gene encodes reactivity to Mls-1a gene products.第三个T细胞受体β链可变区基因编码对Mls-1a基因产物的反应性。
Proc Natl Acad Sci U S A. 1989 Aug;86(16):6293-6. doi: 10.1073/pnas.86.16.6293.
7
Positive and negative selection of Tcrb-V6+ T cells.
Immunogenetics. 1992;36(4):230-7. doi: 10.1007/BF00215053.
8
An exogenous mouse mammary tumor virus with properties of Mls-1a (Mtv-7).一种具有Mls-1a（Mtv-7）特性的外源性小鼠乳腺肿瘤病毒。
J Exp Med. 1992 Jun 1;175(6):1623-33. doi: 10.1084/jem.175.6.1623.
9
Mls-1-like superantigen in the MA/MyJ mouse is encoded by a new mammary tumor provirus that is distinct from Mtv-7.MA/MyJ小鼠中的Mls-1样超抗原由一种新的乳腺肿瘤前病毒编码，该病毒与Mtv-7不同。
J Exp Med. 1992 Jun 1;175(6):1613-21. doi: 10.1084/jem.175.6.1613.