Peripheral blood T cell expansions in patients with Behcet's disease
Peripheral blood T cell expansions in patients with Behcet's disease
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DOI：
10.1046/j.1365-2249.1997.d01-947.x
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发表时间：
1997-03-01
影响因子：
4.6
通讯作者：
Wigzell, H
中科院分区：
文献类型：
--
作者：
Esin, S;Gul, A;Wigzell, H
白塞氏病（ED）是一种慢性多系统炎症性疾病，主要以复发性口腔和生殖器溃疡和葡萄膜炎为特征。ED的病因和发病机制尚不清楚。分析T细胞受体（TCR） V α /N β基因产物及J β基因片段在BD患者外周血中的表达，探讨T淋巴细胞在BD发病中的可能作用。采用12种TCRV特异性MoAbs进行TCRV分析。通过聚合酶链反应（PCR）技术，使用V β和C β特异性引物，对PCR产物进行Southern印迹，随后与放射性标记的J β基因片段特异性探针杂交，确定表达特定V β s的T细胞群体对J β基因片段的使用。虽然23例ED患者中有13例表现出一种或多种TCR v基因产物的表达增加，但ED患者中只有CD4(+) T细胞亚群的扩增（7/23）比健康对照组（0/15）明显更频繁（P = 0.019）。在随访长达20个月的8例病例中，有6例至少有一次与疾病活动相关的扩张。在所有分析的T细胞扩增中，对特定J β基因片段的严格偏好暗示了克隆性，并且与疾病活动密切相关。这些结果提示抗原特异性T淋巴细胞可能参与ED的发病机制。
Behcet's disease (ED) is a chronic multisystemic inflammatory disorder characterized mainly by recurrent oral and genital aphthous ulcerations and uveitis. Etiology and pathogenesis of ED remain unknown. T cell receptor (TCR) V alpha/N beta gene product expression as well as J beta gene segment expression in peripheral blood of BD patients were analysed to investigate the possible role of T lymphocytes in the etiopathogenesis of BD. Flow cytometry with 12 TCR V-specific MoAbs was used for TCRV analyses. J beta gene segment usage by T cell populations expressing certain V beta s was determined by polymerase chain reaction (PCR) technique with V beta- and C beta-specific primers, Southern blotting of PCR products, and subsequent hybridization with radiolabelled J beta gene segment-specific probes. Although 13 of the 23 ED patients exhibited increases in expression of one or more TCR V-gene products, only expansions among the CD4(+) T cell subset were significantly more frequent in ED patients (7/23) compared with healthy controls (0/15) (P = 0.019). Six out of eight cases followed for up to 20 months had at least one expansion correlated with disease activity. A strict preference for particular J beta gene segments implicating clonality was apparent in all analysed T cell expansions and correlated well with disease activity. These results suggest a possible involvement of antigen-specific T lymphocytes in the pathogenesis of ED.