Rochet N, Blanche S, Carel J C, Fischer A, Deist F L, Griscelli C, Van Obberghen E, Le Marchand-Brustel Y
INSERM U145, Faculté de Médecine, Nice, France.
Diabetologia. 1989 Mar;32(3):167-72. doi: 10.1007/BF00265089.
Severe hypoglycaemia developed seven months after a bone marrow transplantation in a child with severe combined immunodeficiency. His serum exerted potent insulin-like activity: (a) it stimulated insulin receptor autophosphorylation and kinase activity in cell-free systems, this effect being additive to insulin; (b) it increased glucose transport in isolated soleus muscle. These insulin-like effects were due to immunoglobulins against the insulin receptor. Indeed, the patient serum immunoprecipitated human or murine insulin receptors from different tissues and inhibited insulin binding to receptor on human IM-9 lymphocytes. After corticoids and immunosuppressive therapy by azathioprine, the patient hypoglycaemic episodes disappeared, and concomitantly, the antibodies to insulin receptor were no longer detected, as judged by both immunoprecipitation of insulin receptor and stimulation of glucose transport.
一名患有严重联合免疫缺陷的儿童在骨髓移植七个月后出现严重低血糖。其血清具有强大的胰岛素样活性：(a) 在无细胞系统中刺激胰岛素受体自身磷酸化和激酶活性，这种作用与胰岛素相加；(b) 增加离体比目鱼肌中的葡萄糖转运。这些胰岛素样作用归因于抗胰岛素受体的免疫球蛋白。实际上，患者血清能从不同组织中免疫沉淀人或小鼠胰岛素受体，并抑制胰岛素与人IM-9淋巴细胞上受体的结合。经皮质类固醇和硫唑嘌呤免疫抑制治疗后，患者低血糖发作消失，同时，通过胰岛素受体免疫沉淀和葡萄糖转运刺激判断，不再检测到胰岛素受体抗体。
