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1
Expression of a transgenic T cell receptor beta chain enhances collagen-induced arthritis.转基因T细胞受体β链的表达增强了胶原诱导的关节炎。
J Exp Med. 1992 Aug 1;176(2):381-8. doi: 10.1084/jem.176.2.381.
2
T-cell receptor vbeta deletion and valpha polymorphism are responsible for the resistance of SWR mouse to arthritis induction.T细胞受体vβ缺失和vα多态性是SWR小鼠对关节炎诱导产生抗性的原因。
Immunogenetics. 1999 Aug;49(9):764-72. doi: 10.1007/s002510050550.
3
T-cell receptor V beta haplotype and complement component C5 play no significant role for the resistance to collagen-induced arthritis in the SWR mouse.T细胞受体Vβ单倍型和补体成分C5在SWR小鼠对胶原诱导性关节炎的抗性中不起显著作用。
Immunology. 1991 Jun;73(2):191-6.
4
Collagen-induced arthritis and TCRs in SWR and B10.Q mice expressing an Ek alpha transgene.表达Ekα转基因的SWR和B10.Q小鼠中的胶原诱导性关节炎及T细胞受体
J Immunol. 1994 Sep 15;153(6):2758-68.
5
Visualization and phenotyping of proinflammatory antigen-specific T cells during collagen-induced arthritis in a mouse with a fixed collagen type II-specific transgenic T-cell receptor β-chain.在固定型 II 型胶原特异性转基因 T 细胞受体 β 链小鼠胶原诱导性关节炎中，促炎性抗原特异性 T 细胞的可视化和表型分析。
Arthritis Res Ther. 2010;12(4):R155. doi: 10.1186/ar3108. Epub 2010 Aug 3.
6
Expression of an ovalbumin-specific V beta 8.2 TCR transgene inhibits collagen arthritis in B10.Q mice.卵清蛋白特异性Vβ8.2 TCR转基因的表达可抑制B10.Q小鼠的胶原性关节炎。
Int Immunol. 1995 Aug;7(8):1279-86. doi: 10.1093/intimm/7.8.1279.
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T cell receptors recognizing type II collagen in HLA-DR-transgenic mice characterized by highly restricted V beta usage.在以高度受限的Vβ使用为特征的HLA - DR转基因小鼠中识别II型胶原蛋白的T细胞受体。
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Epitope glycosylation plays a critical role for T cell recognition of type II collagen in collagen-induced arthritis.表位糖基化在胶原诱导性关节炎中对T细胞识别II型胶原起着关键作用。
Eur J Immunol. 1998 Aug;28(8):2580-90. doi: 10.1002/(SICI)1521-4141(199808)28:08<2580::AID-IMMU2580>3.0.CO;2-X.
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T cell regulation of collagen-induced arthritis in mice. III. Is T cell vaccination a valuable therapy?小鼠中胶原诱导性关节炎的T细胞调节。III. T细胞疫苗接种是一种有价值的治疗方法吗？
Eur J Immunol. 1994 Nov;24(11):2775-83. doi: 10.1002/eji.1830241130.
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Influence of complement C5 and V beta T cell receptor mutations on susceptibility to collagen-induced arthritis in mice.补体C5和VβT细胞受体突变对小鼠胶原诱导性关节炎易感性的影响。
J Immunol. 1989 Apr 1;142(7):2237-43.

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T Cell Receptor Chain Centricity: The Phenomenon and Potential Applications in Cancer Immunotherapy.T 细胞受体链偏倚性：现象及其在癌症免疫治疗中的潜在应用。
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CTLA-4 expressed by FOXP3 regulatory T cells prevents inflammatory tissue attack and not T-cell priming in arthritis.由FOXP3调节性T细胞表达的CTLA-4可预防炎症组织攻击，而非关节炎中的T细胞启动。
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Collagen type II and a thermo-responsive polymer of N-isopropylacrylamide induce arthritis independent of Toll-like receptors: a strong influence by major histocompatibility complex class II and Ncf1 genes.Ⅱ型胶原和 N-异丙基丙烯酰胺的热响应聚合物可独立于 Toll 样受体诱导关节炎：主要组织相容性复合体 II 类和 Ncf1 基因的强烈影响。
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Visualization and phenotyping of proinflammatory antigen-specific T cells during collagen-induced arthritis in a mouse with a fixed collagen type II-specific transgenic T-cell receptor β-chain.在固定型 II 型胶原特异性转基因 T 细胞受体 β 链小鼠胶原诱导性关节炎中，促炎性抗原特异性 T 细胞的可视化和表型分析。
Arthritis Res Ther. 2010;12(4):R155. doi: 10.1186/ar3108. Epub 2010 Aug 3.
7
Epicutaneous immunization with type II collagen inhibits both onset and progression of chronic collagen-induced arthritis.皮内免疫 II 型胶原可抑制慢性胶原诱导性关节炎的发病和进展。
PLoS One. 2007 Apr 18;2(4):e387. doi: 10.1371/journal.pone.0000387.
8
Antigen-specific expansion of TCR Vbeta3+ CD4+ T cells in the early stage of collagen-induced arthritis and its arthritogenic role in DBA/1J mice.胶原诱导性关节炎早期TCR Vβ3⁺ CD4⁺ T细胞的抗原特异性扩增及其在DBA/1J小鼠中的致关节炎作用
J Clin Immunol. 2006 May;26(3):204-12. doi: 10.1007/s10875-006-9012-8. Epub 2006 Apr 29.
9
Prevention of arthritis by interleukin 10-producing B cells.产生白细胞介素-10的B细胞对关节炎的预防作用。
J Exp Med. 2003 Feb 17;197(4):489-501. doi: 10.1084/jem.20021293.
10
Intravenous tolerization with type II collagen induces interleukin-4-and interleukin-10-producing CD4+ T cells.用II型胶原蛋白进行静脉耐受诱导产生白细胞介素-4和白细胞介素-10的CD4 + T细胞。
Immunology. 1999 Jul;97(3):466-73. doi: 10.1046/j.1365-2567.1999.00778.x.

本文引用的文献

1
Type II collagen-induced arthritis in mice. I. Major histocompatibility complex (I region) linkage and antibody correlates.小鼠Ⅱ型胶原诱导性关节炎。I. 主要组织相容性复合体（I区）连锁及抗体相关性
J Exp Med. 1981 Sep 1;154(3):688-700. doi: 10.1084/jem.154.3.688.
2
Quantitative studies on T cell diversity. I. Determination of the precursor frequencies for two types of streptococcus A-specific helper cells in nonimmune, polyclonally activated splenic T cells.T细胞多样性的定量研究。I. 非免疫、多克隆激活的脾T细胞中两种A群链球菌特异性辅助细胞前体频率的测定。
J Exp Med. 1980 Sep 1;152(3):477-92. doi: 10.1084/jem.152.3.477.
3
Immunisation against heterologous type II collagen induces arthritis in mice.针对异源II型胶原蛋白进行免疫接种会在小鼠中诱发关节炎。
Nature. 1980 Feb 14;283(5748):666-8. doi: 10.1038/283666a0.
4
Cleavage of structural proteins during the assembly of the head of bacteriophage T4.在噬菌体T4头部组装过程中结构蛋白的切割
Nature. 1970 Aug 15;227(5259):680-5. doi: 10.1038/227680a0.
5
Structural studies on cartilage collagen employing limited cleavage and solubilization with pepsin.利用胃蛋白酶进行有限裂解和溶解对软骨胶原蛋白进行的结构研究。
Biochemistry. 1972 Dec 19;11(26):4903-9. doi: 10.1021/bi00776a005.
6
Experimental arthritis in a nonhuman primate. I. Induction by bovine type II collagen.非人灵长类动物的实验性关节炎。I. 由牛II型胶原诱导产生。
Lab Invest. 1986 Jan;54(1):26-31.
7
Genetic susceptibility to murine collagen II autoimmune arthritis. Proposed relationship to the IgG2 autoantibody subclass response, complement C5, major histocompatibility complex (MHC) and non-MHC loci.小鼠胶原II型自身免疫性关节炎的遗传易感性。与IgG2自身抗体亚类反应、补体C5、主要组织相容性复合体（MHC）和非MHC基因座的潜在关系。
J Exp Med. 1985 Dec 1;162(6):1878-91. doi: 10.1084/jem.162.6.1878.
8
Murine T-cell receptor mutants with deletions of beta-chain variable region genes.具有β链可变区基因缺失的小鼠T细胞受体突变体。
Proc Natl Acad Sci U S A. 1986 Feb;83(3):767-71. doi: 10.1073/pnas.83.3.767.
9
The T-cell repertoire is heavily influenced by tolerance to polymorphic self-antigens.T细胞库受到对多态性自身抗原耐受性的严重影响。
Nature. 1988 Oct 27;335(6193):796-801. doi: 10.1038/335796a0.
10
In transgenic mice the introduced functional T cell receptor beta gene prevents expression of endogenous beta genes.在转基因小鼠中，导入的功能性T细胞受体β基因会阻止内源性β基因的表达。
Cell. 1988 Mar 25;52(6):831-41. doi: 10.1016/0092-8674(88)90425-4.

转基因T细胞受体β链的表达增强了胶原诱导的关节炎。

Expression of a transgenic T cell receptor beta chain enhances collagen-induced arthritis.

作者信息

Mori L, Loetscher H, Kakimoto K, Bluethmann H, Steinmetz M

机构信息

Pharmaceutical Research New Technologies, F. Hoffmann-La Roche, Ltd., Basel, Switzerland.

出版信息

J Exp Med. 1992 Aug 1;176(2):381-8. doi: 10.1084/jem.176.2.381.

DOI:10.1084/jem.176.2.381
PMID:1386871
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2119315/
Abstract

SWR/J transgenic (tg) mice were generated expressing the TCR beta chain derived from an anticollagen type II (CII) arthritogenic T cell clone. The SWR/J strain was selected because it is resistant to collagen-induced arthritis (CIA) and lacks the V beta gene segment used by the T cell clone. Expression of the tg beta chain on all thymocytes and peripheral lymph node T cells led to a more efficient anti-CII immune response, but did not confer CIA susceptibility to SWR/J mice. Nevertheless, this tg beta chain enhanced predisposition to CIA as (DBA/1 x SWR) F1 beta tg mice were more susceptible than normal F1 littermates. Our results demonstrate that the expression of the tg beta chain contributes to CIA susceptibility, but by itself it is not sufficient to overcome CIA resistance in the SWR/J strain.

摘要

构建了表达源自抗II型胶原（CII）致关节炎T细胞克隆的TCRβ链的SWR/J转基因（tg）小鼠。选择SWR/J品系是因为它对胶原诱导的关节炎（CIA）具有抗性，并且缺乏该T细胞克隆所使用的Vβ基因片段。tgβ链在所有胸腺细胞和外周淋巴结T细胞上的表达导致了更有效的抗CII免疫反应，但并未使SWR/J小鼠对CIA易感。然而，由于（DBA/1×SWR）F1βtg小鼠比正常F1同窝小鼠更易感，这种tgβ链增强了对CIA的易感性。我们的结果表明，tgβ链的表达有助于CIA易感性，但仅凭其自身不足以克服SWR/J品系对CIA的抗性。