Glinski W, Stepien-Sopniewska B, Korczak-Kowalska G, Glinska-Ferenz M, Gorski A
Department of Dermatology, Warsaw School of Medicine, Poland.
Acta Derm Venereol. 1995 Sep;75(5):353-6. doi: 10.2340/0001555575353356.
Patients with atopic dermatitis were found to have an about 7-fold increased spontaneous proliferative response of peripheral blood lymphocytes and an about 4-fold elevation of CD3-dependent lymphocyte transformation as compared to normal controls. The CD3-dependent lymphocyte response in patients with severe atopic dermatitis lesions was increased to a lower degree than in those with mild skin lesions. Despite a highly increased CD3-dependent lymphocyte response, the extracellular matrix proteins could induce further co-stimulation of lymphocytes in patients with atopic dermatitis, similar to that in normal controls. However, co-activation by type IV collagen was markedly increased in patients with severe lesions, whereas co-stimulations by both type I collagen and fibronectin were decreased in patients with mild lesions. This finding reflects presumably the changes in lymphocyte subpopulations and their activities related to the recirculation of these cells through the active skin lesions and to the contact of T cells with extracellular matrix proteins. The percentage of CD26-positive lymphocytes was also significantly (p < 0.05) increased in patients with severe atopic dermatitis. These data indicate that helper T cells are excessively activated in atopic dermatitis and that the function of beta-1-integrin receptors underlying the extracellular matrix protein-mediated co-activation of CD3-dependent lymphocyte responses is modified by disease severity.
与正常对照组相比,特应性皮炎患者外周血淋巴细胞的自发增殖反应增加约7倍,CD3依赖性淋巴细胞转化升高约4倍。重度特应性皮炎皮损患者的CD3依赖性淋巴细胞反应增加程度低于轻度皮肤损害患者。尽管CD3依赖性淋巴细胞反应高度增加,但细胞外基质蛋白可诱导特应性皮炎患者的淋巴细胞进一步共刺激,类似于正常对照组。然而,IV型胶原的共激活在重度皮损患者中显著增加,而I型胶原和纤连蛋白的共刺激在轻度皮损患者中减少。这一发现可能反映了淋巴细胞亚群及其活性的变化,这些变化与这些细胞通过活动性皮肤损害的再循环以及T细胞与细胞外基质蛋白的接触有关。重度特应性皮炎患者CD26阳性淋巴细胞的百分比也显著增加(p<0.05)。这些数据表明,特应性皮炎中辅助性T细胞过度活化,并且细胞外基质蛋白介导的CD3依赖性淋巴细胞反应共激活所依赖的β-1整合素受体功能因疾病严重程度而改变。