Muscat C, Bertotto A, Agea E, Bistoni O, Ercolani R, Tognellini R, Spinozzi F, Cesarotti M, Gerli R
Institute of Internal Medicine and Oncologic Sciences, University of Perugia, Italy.
Clin Exp Immunol. 1994 Nov;98(2):252-6. doi: 10.1111/j.1365-2249.1994.tb06134.x.
The expression and the functional role of the CD26 (1F7) T cell surface molecule, an ectoenzyme which seems to represent a functional collagen receptor of T lymphocytes and to have a role in T cell activation, were analysed in both peripheral blood (PB) and synovial fluid (SF) T cell samples from patients with active and inactive rheumatoid arthritis (RA). Although patients with active disease displayed higher percentages of PB CD26+ CD4+ T cells than inactive RA and control subjects, CD26 antigen expression on RA SF T lymphocytes was low. The anti-1F7 binding to the T cell surface, that led to CD26 antigen modulation and enhancement of both IL-2 synthesis by, and 3H-TdR incorporation of, anti-CD3- or anti-CD2-triggered PB T cells in RA and control subjects, was unable to affect significantly both expression and functional activity of RA SF T lymphocytes. Since the 1F7 antigen spontaneously reappeared on the surface of unstimulated SF T cells after 2-5 days of culturing, the low 1F7 antigen expression of anti-1F7 in the SF T cell compartment may be the result of in vivo molecule modulation exerted by the natural ligand in the joint, with important implications for T cell activation and lymphokine synthesis.
对CD26（1F7）T细胞表面分子的表达及其功能作用进行了分析，该分子是一种外切酶，似乎是T淋巴细胞的功能性胶原受体，并在T细胞活化中起作用。研究对象为患有活动期和非活动期类风湿性关节炎（RA）的患者的外周血（PB）和滑液（SF）中的T细胞样本。尽管活动期疾病患者外周血中CD26 + CD4 + T细胞的百分比高于非活动期RA患者和对照组，但类风湿性关节炎滑液T淋巴细胞上的CD26抗原表达较低。在类风湿性关节炎患者和对照组中，抗1F7与T细胞表面结合，导致CD26抗原调节，并增强抗CD3或抗CD2触发的外周血T细胞的IL-2合成和3H-TdR掺入，但无法显著影响类风湿性关节炎滑液T淋巴细胞的表达和功能活性。由于在培养2 - 5天后，未刺激的滑液T细胞表面会自发重新出现1F7抗原，因此滑液T细胞区室中抗1F7的低1F7抗原表达可能是关节中天然配体在体内进行分子调节的结果，这对T细胞活化和淋巴因子合成具有重要意义。
