Lernmark A, Sehlin J, Täljedal I B, Kromann H, Nerup J
Diabetologia. 1978 Jan 14;14(1):25-31. doi: 10.1007/BF00429704.
Serum from normal blood-donors and juvenile diabetic patients inhibited Rb+ accumulation and stimulated release of 51Cr and insulin in suspensions of dispersed pancreatic islet cells prepared from ob/ob mouse islets, which are rich in B-cells. The effects indicate the presence of a B-cytotoxic factor in human serum. Serum from mouse and fetal calf also inhibited the islet cell accumulation of Rb+. Toxicity was not suppressed by treating serum with protein A-Sepharose and did not correlate with islet cell binding of fluorescent antibodies to human immunoglobulin. Whereas all sera inhibited Rb+ accumulation, 3 of 6 diabetic patient sera, but no blood-donor serum, made the cells fluoresce on exposure to the fluorescent antibodies. Supporting a dependence on complement, toxicity remained after dialysis, but was destroyed by treating serum with zymosan-A or heating at 56 degrees for 30 min.
来自正常献血者和青少年糖尿病患者的血清,抑制了从富含β细胞的ob/ob小鼠胰岛制备的分散胰岛细胞悬液中Rb⁺的积累,并刺激了⁵¹Cr和胰岛素的释放。这些效应表明人血清中存在一种β细胞毒性因子。小鼠血清和胎牛血清也抑制了胰岛细胞对Rb⁺的摄取。用蛋白A-琼脂糖处理血清并不能抑制毒性,且毒性与胰岛细胞对人免疫球蛋白荧光抗体的结合无关。尽管所有血清都抑制了Rb⁺的积累,但6例糖尿病患者血清中有3例,而献血者血清中没有,使细胞在接触荧光抗体后发出荧光。支持补体依赖性,透析后毒性仍然存在,但用酵母聚糖-A处理血清或在56℃加热30分钟可破坏毒性。