Li X
PUMC Hospital, Beijing.
Zhongguo Yi Xue Ke Xue Yuan Xue Bao. 1993 Apr;15(2):83-8.
Using the immunohistochemical avidin-biotin-peroxidase complex (ABC) method, lymphocyte subsets in the salivary glands of 15 patients with primary Sjogren's syndrome, 7 patients with secondary Sjogren's syndrome and 4 normal controls were identified by monoclonal antibodies. The infiltrating lymphocytes were mainly T lymphocytes, the majority of which were T helper cells (Leu-3a) in SS groups. The Leu-3a/Leu-2a ratio was increased. These changes were related to the degrees of the disease. The lymphocytes of patients expressed the HLA-DR antigen (Ia). Thus genetic predisposition plays an important role in the disease. A proposed mechanism is that the deficiency of suppressor lymphocytes and the overactivity of helper lymphocytes would result in B cells becoming hyperactive. Multiple autoantibodies produced by the B cells would contribute to tissue damage, and the tissue fragments would in turn further stimulate antibody production.
采用免疫组织化学抗生物素蛋白-生物素-过氧化物酶复合物（ABC）法，用单克隆抗体鉴定了15例原发性干燥综合征患者、7例继发性干燥综合征患者及4例正常对照者唾液腺中的淋巴细胞亚群。浸润的淋巴细胞主要为T淋巴细胞，在干燥综合征组中大多数为辅助性T细胞（Leu-3a）。Leu-3a/Leu-2a比值升高。这些变化与疾病程度相关。患者的淋巴细胞表达HLA-DR抗原（Ia）。因此，遗传易感性在该疾病中起重要作用。一种推测的机制是，抑制性淋巴细胞缺陷和辅助性淋巴细胞过度活跃会导致B细胞变得活跃。B细胞产生的多种自身抗体将导致组织损伤，而组织碎片又会进一步刺激抗体产生。
