Brownlee M, Pongor S, Cerami A
J Exp Med. 1983 Nov 1;158(5):1739-44. doi: 10.1084/jem.158.5.1739.
The chronic tissue damage associated with long-term diabetes mellitus may arise in part from in situ immune complex formation by accumulated immunoglobulins and/or antigens bound to long-lived structural proteins that have undergone excessive nonenzymatic glycosylation. In this report, we have tested this hypothesis using nonenzymatically glycosylated collagen. Binding of both albumin and IgG averaged four times the amount bound to unmodified collagen. Both albumin and IgG (anti-BSA) bound to nonenzymatically glycosylated collagen retained their ability to form immune complexes in situ with free antibody and antigen.
与长期糖尿病相关的慢性组织损伤可能部分源于原位免疫复合物的形成，这些复合物由积累的免疫球蛋白和/或与经历了过度非酶糖基化的长寿结构蛋白结合的抗原组成。在本报告中，我们使用非酶糖基化胶原蛋白对这一假设进行了验证。白蛋白和IgG的结合量平均是与未修饰胶原蛋白结合量的四倍。与非酶糖基化胶原蛋白结合的白蛋白和IgG（抗牛血清白蛋白）均保留了与游离抗体和抗原原位形成免疫复合物的能力。
