Oligoclonal accumulations of T-cell clones in gingivitis and periodontitis lesions.
Oligoclonal accumulations of T-cell clones in gingivitis and periodontitis lesions.
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牙龈炎和牙周炎病变中 T 细胞克隆的寡克隆积累。
DOI：
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发表时间：
2002
影响因子：
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通讯作者：
K. Yamazaki
中科院分区：
文献类型：
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作者：
H. Itoh;Y. Ohsawa;H. Yoshie;K. Yamazaki
牙周炎和牙周炎具有不同的临床和免疫病理特征。我们以前已经证明，T细胞浸润性牙周炎病变识别有限的抗原或抗原表位。然而，T细胞在牙周炎病变中的克隆性尚不清楚。因此，我们利用逆转录-聚合酶链式反应和单链构象多态性(SSCP)分析相结合的方法对牙周炎病变中的T细胞进行了克隆分析。与牙周炎病变一样，SSCP分析显示出现了许多不同的条带，表明牙周炎病变中有克隆性聚集。虽然牙龈组织的平均条带数显著高于外周血单核细胞，但数值分析清楚地表明，不同疾病类型的牙龈组织标本的条带总数并无差异。虽然每个Vbeta家系中不同条带的数量略有不同，但在牙周炎病变和牙周炎病变之间没有显著差异。这些结果表明，抗原特异性T细胞反应也发生在牙周炎病变中。然而，这些抗原特异的T细胞在牙周病的发病机制中扮演着什么角色，以及这些T细胞识别哪些抗原仍有待确定。
Gingivitis and periodontitis have distinct clinical and immunopathological characteristics. We have previously demonstrated that T cells infiltrating periodontitis lesions recognize a restricted repertoire of antigens or antigenic epitopes. However, the clonality of T cells in the gingivitis lesion is not known. Therefore, we carried out a clonal analysis of T cells infiltrating gingivitis lesions using combined reverse transcription-polymerase chain reaction and single-strand conformation polymorphism (SSCP) analysis. As with periodontitis lesions, SSCP analysis demonstrated the emergence of a number of distinct bands suggesting clonal accumulation in the gingivitis lesion. Although the mean number of distinct bands in gingival tissue was significantly higher than that in peripheral blood mononuclear cells, numerical analysis clearly demonstrated that there was no difference in the total number of bands in gingival tissue specimens between the different disease types. Although there were slight variations in the number of distinct bands in each Vbeta family, there was no significant difference between gingivitis lesions and periodontitis lesions. These results demonstrate that antigen-specific T-cell responses also take place in gingivitis lesions. It remains to be determined, however, what role these antigen-specific T cells play and what antigens the T cells recognize in the pathogenesis of periodontal disease.