Transfer of rheumatoid arthritis into severe combined immunodeficient mice. The pathogenetic implications of T cell populations oligoclonally expanding in the rheumatoid joints.
Transfer of rheumatoid arthritis into severe combined immunodeficient mice. The pathogenetic implications of T cell populations oligoclonally expanding in the rheumatoid joints.
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将类风湿性关节炎转移到严重联合免疫缺陷小鼠中。
DOI：
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发表时间：
1995
影响因子：
15.9
通讯作者：
Tadamitsu Kishimoto
中科院分区：
文献类型：
--
作者：
T. Mima;Y. Saeki;S. Ohshima;N. Nishimoto;Masato Matsushita;M. Shimizu;Yasushi Kobayashi;Tatsuji Nomura;Tadamitsu Kishimoto
为了研究T细胞浸润类风湿关节的致病性，从RA患者的滑液或滑膜组织中分离的单核细胞（MNC），主要是T细胞，通过关节内注射转移到严重联合免疫缺陷（SCID）小鼠中。根据我们在这个实验系统中的观察，RA患者至少可以分为两组。在一组患者中，浸润的MNC诱导了受体SCID小鼠（阳性组）的滑膜增生。而在另一组中未观察到滑膜增生（阴性组）。在阳性组中观察到的滑膜增生的诱导被抗人CD 3抗体（OKT 3）阻止，表明T细胞介导。通过逆转录聚合酶链反应分析转移到SCID小鼠的浸润性MNC中的T细胞受体（TCR）V β的使用情况，发现仅在阳性组中优先使用某些V β基因，而在外周血MNC中未观察到。TCR/V β偏斜的模式在患者中不一致。PCR扩增的TCR/ V β基因单链构象多态性分析显示，阳性组类风湿关节中扩增的T细胞群为寡克隆性。此外，通过用相关超抗原体外刺激患者的外周血MNC，表达这种偏斜TCR/V β的T细胞群的富集能够诱导SCID小鼠中的滑膜增生。这些结果表明，致病性T细胞可以激活局部在类风湿关节的某些抗原在一些，但不是在所有的RA患者。
To investigate the pathogenicity of T cells infiltrating in the rheumatoid joints, mononuclear cells (MNC), predominantly T cells, isolated from either synovial fluid or synovial tissues of the patients with RA were transferred into severe combined immunodeficient (SCID) mice by intraarticular injections. According to our observations in this experimental system, patients with RA could be classified into at least two groups. In one group of patients, the infiltrating MNC induced synovial hyperplasia in the recipient SCID mice (the positive group). Whereas, in the other group no synovial hyperplasia was observed (the negative group). The induction of synovial hyperplasia observed in the positive group was prevented by an anti-human CD3 antibody (OKT3), indicating T cell mediation. Analysis of T cell receptor (TCR) V beta usage by reverse transcriptase polymerase chain reaction in the infiltrating MNC transferred into SCID mice revealed a marked skew towards the preferential use of certain V beta genes, which was not seen in the peripheral blood MNC, in only the positive group. The patterns of TCR/V beta skew were not uniform among the patients. The analysis of the PCR-amplified genes of such skewed TCR/ V beta by single strand conformational polymorphism showed distinct bands, indicating that the T cell populations expanding in rheumatoid joints of the positive group were oligoclonal. Furthermore, the enrichment of the T cell populations expressing such skewed TCR/V beta by in vitro stimulation of peripheral blood MNC of the patients with the relevant superantigen enabled the induction of synovial hyperplasia in the SCID mice. These results suggest that the pathogenic T cells could be activated locally in rheumatoid joints by certain antigens in some, but not in all patients with RA.
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影响因子：
56.9
作者：
MCCUNE, JM;NAMIKAWA, R;WEISSMAN, IL
通讯作者：
WEISSMAN, IL
影响因子：
56.9
作者：
PALIARD, X;WEST, SG;KOTZIN, BL
通讯作者：
KOTZIN, BL
急性传染性单核细胞增多症刺激 V beta 6.1-3 和 V beta 7 T 细胞的选择性表达/扩增。
影响因子：
20.3
作者：
Smith,TJ;Terada,N;Robinson,CC;Gelfand,EW
通讯作者：
Gelfand,EW
关节炎中 T 淋巴细胞浸润的克隆优势。
DOI：
10.1073/pnas.85.4.1179
发表时间：
1988
影响因子：
11.1
作者：
Stamenkovic,I;Stegagno,M;Wright,KA;Krane,SM;Amento,EP;Colvin,RB;Duquesnoy,RJ;Kurnick,JT
通讯作者：
Kurnick,JT