Campbell I L, Bizilj K, Colman P G, Tuch B E, Harrison L C
J Clin Endocrinol Metab. 1986 Jun;62(6):1101-9. doi: 10.1210/jcem-62-6-1101.
We examined the effect of interferon-gamma (IFN gamma) on expression of the major histocompatibility proteins on cultured human islet cells isolated from adult and fetal pancreas and from an insulinoma. While the pancreatic beta-cells from different sources varied in their responses to IFN gamma, in all instances the expression of HLA-A,B,C protein was increased. Pancreatic beta-cells did not express HLA-DR protein, before or after culture of the islets in IFN gamma, although HLA-DR protein expression was induced on some non-beta-cells. These findings are at variance with those reported with thyroid follicular cells, in which IFN gamma induced expression of HLA-DR. We, therefore, conclude that the interaction between the immune and the endocrine systems may be endocrine cell specific. The up-regulation of HLA-A,B,C protein on beta-cells by IFN gamma provides a mechanism for enhanced targetting to the beta-cells of autoreactive cytotoxic T-lymphocytes and, hence, for amplifying beta-cell destruction.
我们研究了γ干扰素(IFNγ)对从成人及胎儿胰腺以及胰岛素瘤中分离出的培养人胰岛细胞上主要组织相容性蛋白表达的影响。虽然来自不同来源的胰腺β细胞对IFNγ的反应有所不同,但在所有情况下,HLA - A、B、C蛋白的表达均增加。胰岛在IFNγ中培养前后,胰腺β细胞均不表达HLA - DR蛋白,尽管在一些非β细胞上可诱导HLA - DR蛋白表达。这些发现与甲状腺滤泡细胞的报道结果不同,在甲状腺滤泡细胞中IFNγ可诱导HLA - DR表达。因此,我们得出结论,免疫和内分泌系统之间的相互作用可能具有内分泌细胞特异性。IFNγ使β细胞上的HLA - A、B、C蛋白上调,为自身反应性细胞毒性T淋巴细胞增强靶向β细胞提供了一种机制,从而加剧β细胞的破坏。