Romano M F, Turco M C, Stanziola A, Giarrusso P C, Petrella A, Tassone P, van Lier R, Venuta S, Formisano S
Dipartimento di Biologia e Patologia Cellulare e Molecolare, II Facoltà di Medicina e Chirurgia, Università di Napoli, Italia.
Cell Immunol. 1993 May;148(2):455-63. doi: 10.1006/cimm.1993.1127.
We previously reported that T lymphocytes of atopic patients displayed a defect in CD2- and CD3-mediated pathways of cell activation; that defect relied on impairment of interleukin 2 (IL-2) production (Romano, M. F., Valerio, G., Turco, M. C., Spadaro, G., Venuta, S., and Formisono, S., Cell. Immunol. 139, 91, 1992). We have subsequently analyzed T cell response to anti-CD2, -CD3, or -CD28 monoclonal antibodies (mAb) in 40 atopic individuals, including patients subjected to immunotherapy. In the latter group T cell response to anti-CD2 mAbs was normal, while IL-2 production and proliferative response in T lymphocytes stimulated via CD3 was still impaired. Costimulation with anti-CD28 mAb rescued both IL-2 production and proliferative response in all tested patients. Response to CD28-mediated stimulation was more pronounced in atopic than that in normal individuals. Our results indicated that CD28 had a major role in T cell proliferation of atopic patients and provided a model for analyzing CD3/CD28 interactions in regulation of IL-2 gene expression.
我们先前报道过，特应性患者的T淋巴细胞在CD2和CD3介导的细胞激活途径中存在缺陷；该缺陷依赖于白细胞介素2（IL-2）产生的受损（Romano, M. F., Valerio, G., Turco, M. C., Spadaro, G., Venuta, S., and Formisono, S., Cell. Immunol. 139, 91, 1992）。我们随后分析了40名特应性个体（包括接受免疫疗法的患者）的T细胞对抗CD2、-CD3或-CD28单克隆抗体（mAb）的反应。在后一组中，T细胞对抗CD2 mAb的反应正常，而通过CD3刺激的T淋巴细胞中的IL-2产生和增殖反应仍然受损。用抗CD28 mAb进行共刺激可挽救所有受试患者的IL-2产生和增殖反应。特应性个体对CD28介导刺激的反应比正常个体更明显。我们的结果表明，CD28在特应性患者的T细胞增殖中起主要作用，并为分析CD3/CD28相互作用对IL-2基因表达的调节提供了一个模型。
