人T细胞白血病病毒I型Env-pX转基因小鼠中Env/Tax蛋白自身抗原的证据。
Evidence for autoantigens of Env/Tax proteins in human T cell leukemia virus type I Env-pX transgenic mice.
作者信息
Fujisawa K, Okamoto K, Asahara H, Hasunuma T, Kobata T, Kato T, Sumida T, Nishioka K
机构信息
St. Marianna University School of Medicine, Kawasaki, Japan.
出版信息
Arthritis Rheum. 1998 Jan;41(1):101-9. doi: 10.1002/1529-0131(199801)41:1<101::AID-ART13>3.0.CO;2-L.
OBJECTIVE
To examine T cell clonotypes infiltrating into arthritic joints and to investigate whether human T cell leukemia virus type I (HTLV-I) env-pX gene products act as autoantigens in HTLV-I env-pX transgenic mice.
METHODS
Complementary DNA (cDNA) encoding the V-D-J (third complementarity-determining region [CDR3]) region of T cell receptor beta chain was amplified by Vbeta family polymerase chain reaction. T cell clonotypes were detected by a single-strand conformational polymorphism method, and sequence analysis of the CDR3 region was performed.
RESULTS
Distinct oligoclonal T cell expansion was observed in arthritic joints, and a conserved amino acid motif in the CDR3 region was found in T cells infiltrating joints. Moreover, several intraarticular T cells recognized HTLV-I Env and Tax proteins.
CONCLUSION
Our results suggest that HTLV-I Env and Tax proteins act as autoantigens that are recognized by autoreactive T cells in inflamed arthritic lesions in the HTLV-I env-pX transgenic mouse. Thus, some T cells infiltrating the joint recognize Env or Tax protein. These cells may trigger chronic arthritis in HTLV-I env-pX transgenic mice.
目的
检测浸润到关节炎关节中的T细胞克隆型，并研究I型人类T细胞白血病病毒（HTLV-I）env-pX基因产物在HTLV-I env-pX转基因小鼠中是否作为自身抗原。
方法
通过Vβ家族聚合酶链反应扩增编码T细胞受体β链V-D-J（第三个互补决定区[CDR3]）区域的互补DNA（cDNA）。采用单链构象多态性方法检测T细胞克隆型，并对CDR3区域进行序列分析。
结果
在关节炎关节中观察到明显的寡克隆T细胞扩增，并且在浸润关节的T细胞中发现了CDR3区域中的一个保守氨基酸基序。此外，一些关节内T细胞识别HTLV-I Env和Tax蛋白。
结论
我们的结果表明，HTLV-I Env和Tax蛋白作为自身抗原，在HTLV-I env-pX转基因小鼠的炎症性关节炎病变中被自身反应性T细胞识别。因此，一些浸润关节的T细胞识别Env或Tax蛋白。这些细胞可能引发HTLV-I env-pX转基因小鼠的慢性关节炎。
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