González-Amaro R, Baranda L, Abud-Mendoza C, Delgado S P, Moncada B
Department of Immunology, School of Medicine, University of San Luis Potosi, Mexico.
J Am Acad Dermatol. 1993 Jan;28(1):56-60. doi: 10.1016/0190-9622(93)70009-i.
The pathogenesis of autoeczematization (AE) is not well understood; however, previous studies suggest that AE is an autoimmune condition.
Our purpose was to assess whether AE is associated with an abnormal immune recognition of autologous skin antigens.
Eight patients with AE, six healthy control subjects, and three patients with localized contact dermatitis (LCD) were studied. Activation markers were detected on peripheral blood T lymphocytes. Autologous mixed epidermal cell-lymphocyte reaction (AMECLR) was performed for each subject and cell proliferation was assessed by tritiated thymidine incorporation.
Many activated T cells were detected in patients with AE (5.2% +/- 4.5% vs 0.2% +/- 0.4% in control subjects, p < 0.05). AMECLR showed a significantly higher cell proliferation in AE compared with both healthy subjects and patients with LCD (6372 +/- 3217 cpm vs 2638 +/- 1788 cpm, and 2471 +/- 1389 cpm, respectively; p < 0.05). Peripheral blood mononuclear cells cultured in the presence of an autologous skin homogenate also showed a significantly increased cell proliferation in patients with AE than in control subjects.
Our results suggest that an abnormal immune response against autologous skin antigens occurs in AE that could be related to the pathogenesis of this disease.
自身湿疹化(AE)的发病机制尚未完全明确;然而,既往研究提示AE是一种自身免疫性疾病。
我们的目的是评估AE是否与对自身皮肤抗原的异常免疫识别有关。
研究了8例AE患者、6名健康对照者和3例局限性接触性皮炎(LCD)患者。检测外周血T淋巴细胞上的活化标志物。对每个受试者进行自体混合表皮细胞-淋巴细胞反应(AMECLR),并通过氚化胸腺嘧啶核苷掺入法评估细胞增殖。
在AE患者中检测到许多活化T细胞(5.2%±4.5%,而对照者为0.2%±0.4%,p<0.05)。与健康受试者和LCD患者相比,AMECLR显示AE患者的细胞增殖显著更高(分别为6372±3217 cpm、2638±1788 cpm和2471±1389 cpm;p<0.05)。在自体皮肤匀浆存在的情况下培养的外周血单个核细胞也显示,AE患者的细胞增殖比对照者显著增加。
我们的结果提示,AE中发生了针对自身皮肤抗原的异常免疫反应,这可能与该疾病的发病机制有关。