Jacobson J D, Markmann J F, Brayman K L, Barker C F, Naji A
Department of Surgery, University of Pennsylvania School of Medicine, Philadelphia.
Diabetes. 1988 Jun;37(6):838-41. doi: 10.2337/diab.37.6.838.
BB rats exhibit a syndrome of spontaneous diabetes that has clinical and pathological characteristics analogous to those found in human insulin-dependent diabetes mellitus (IDDM). Islet tissue transplanted into spontaneously diabetic BB rats is uniformly destroyed by a recurrence of the autoimmune response that destroyed the diabetic subject's native islets. To examine recurrent autoimmune destruction of transplanted islets, it is necessary to exclude islet damage that might result from allograft rejection. We utilized neonatal tolerance induction to prevent rejection of Wistar-Furth (WF) (RT1u) islet allografts by spontaneously diabetic BB recipients. We determined that islet-recipient treatment with anti-asialo-GM1 (anti-AGM1) antibody prevents recurrent autoimmune diabetes that would otherwise destroy transplanted WF islet grafts. Anti-AGM1 therapy significantly decreased peripheral blood natural killer (NK) cell activity. These data suggest a role for NK cells in the pathogenesis of recurrent diabetes in neonatally tolerant BB rats.
BB大鼠表现出一种自发性糖尿病综合征,其临床和病理特征与人类胰岛素依赖型糖尿病(IDDM)相似。移植到自发性糖尿病BB大鼠体内的胰岛组织会因自身免疫反应的复发而被一致破坏,这种自身免疫反应曾破坏了糖尿病个体的天然胰岛。为了研究移植胰岛的复发性自身免疫破坏,有必要排除可能由同种异体移植排斥导致的胰岛损伤。我们利用新生期耐受诱导来防止自发性糖尿病BB受体对Wistar-Furth(WF)(RT1u)胰岛同种异体移植的排斥。我们确定用抗唾液酸化GM1(抗-AGM1)抗体治疗胰岛受体可预防复发性自身免疫性糖尿病,否则这种糖尿病会破坏移植的WF胰岛移植物。抗-AGM1疗法显著降低了外周血自然杀伤(NK)细胞活性。这些数据表明NK细胞在新生期耐受的BB大鼠复发性糖尿病发病机制中起作用。