Nouri Aria K T, Lombard M, Williams R
Institute of Liver Studies, King's College School of Medicine and Dentistry, London, England.
Clin Exp Immunol. 1991 Oct;86(1):140-4. doi: 10.1111/j.1365-2249.1991.tb05786.x.
Reduced suppressor cell number and function have been described in a number of autoimmune diseases and this may contribute to pathogenesis. Suppressor cell function depends upon the interaction of the CD8 antigen expressed on suppressor cells with other limbs of the immune system. Recently, soluble membrane antigens including CD8 have been identified in serum and it is possible that the loss of such antigens from viable cells could result in functional deficit. In order to examine whether the decreased suppressor cell function reported in autoimmune type of chronic liver disease is associated with soluble serum CD8 levels, sera from 23 patients with primary biliary cirrhosis (PBC), 12 with autoimmune chronic active hepatitis (AI-CAH) and 21 healthy controls were tested using a commercially available enzyme immunoassay. The proportion of cells expressing the CD8 antigen and the intensity of its display were also determined using an immunofluorescent technique and an ELISA, respectively, for 12 PBC and 10 healthy controls. The soluble serum CD8 levels were significantly higher in PBC (mean U/ml +/- s.d., 777 +/- 331), and AI-CAH (575 +/- 291) than controls (322 +/- 115) (P less than 0.001 and P = 0.004, respectively). While the intensity of CD8 antigen expression on suppressor/cytotoxic populations was not significantly different in PBC (347 +/- 125 per 10(4) cells) compared with controls (441 +/- 206), the mean proportion of CD8 positive cells was significantly less in PBC (14.1 +/- 6.8%) than controls (20 +/- 4.7%) (P less than 0.05). These data suggest that the apparent reduction in suppressor cell number found for patients with PBC and AI-CAH may be a consequence of the shedding or secretion of CD8 antigen from cell membrane of CD8 positive lymphocyte. It is also possible that the loss of this antigen is responsible for the reduced suppressor cell function seen in these conditions.
在许多自身免疫性疾病中,抑制细胞数量减少且功能异常,这可能与发病机制有关。抑制细胞的功能取决于抑制细胞表面表达的CD8抗原与免疫系统其他部分的相互作用。最近,血清中已鉴定出包括CD8在内的可溶性膜抗原,活细胞中此类抗原的缺失可能导致功能缺陷。为了研究自身免疫性慢性肝病中报道的抑制细胞功能下降是否与血清可溶性CD8水平有关,我们使用市售酶免疫测定法检测了23例原发性胆汁性肝硬化(PBC)患者、12例自身免疫性慢性活动性肝炎(AI-CAH)患者和21名健康对照者的血清。对于12例PBC患者和10名健康对照者,我们还分别使用免疫荧光技术和酶联免疫吸附测定法(ELISA)测定了表达CD8抗原的细胞比例及其表达强度。PBC患者(平均U/ml±标准差,777±331)和AI-CAH患者(575±291)的血清可溶性CD8水平显著高于对照组(322±115)(P分别小于0.001和P = 0.004)。虽然PBC患者抑制/细胞毒性群体上CD8抗原的表达强度(每10⁴个细胞347±125)与对照组(441±206)相比无显著差异,但PBC患者CD8阳性细胞的平均比例(14.1±6.8%)显著低于对照组(20±4.7%)(P小于0.05)。这些数据表明,PBC和AI-CAH患者抑制细胞数量的明显减少可能是CD8阳性淋巴细胞细胞膜上CD8抗原脱落或分泌的结果。在这些情况下,这种抗原的缺失也可能是抑制细胞功能降低的原因。