Parkkonen P, Hyöty H, Koskinen L, Leinikki P
Institute of Biomedical Sciences, University of Tampere, Finland.
Diabetologia. 1992 Jan;35(1):63-9. doi: 10.1007/BF00400853.
The ability of mumps virus to infect pancreatic Beta cells and cause alterations in their HLA expression was evaluated in cultured human fetal islet cell clusters. Mumps virus could be isolated during the whole culture period (6-8 days) and 60% of cells, including Beta cells, contained viral nucleocapsid protein at the end of the culturing. A minor decrease in insulin secretion was observed in some of the infected cultures. The infection was invariably associated with an increase in the expression of HLA class I molecules. This enhancement was mediated by soluble factors secreted by infected cells. The infection could not induce the expression of HLA-DR molecules. However, external interferon-gamma was able to cause a clear rise in DR-expression which was observed only on non-Beta-cells. Rubella and coxsackie B4 viruses were also able to enhance the expression of class I molecules while herpes simplex virus type 2 was not. The results suggest that certain viruses are able to infect Beta cells and cause alterations in their immunological appearance. Increased HLA class I expression in infected islets may exaggerate the autoimmune process in pre-diabetic individuals by increasing the activity of autoreactive cytotoxic T cells.
在培养的人胎儿胰岛细胞团中评估了腮腺炎病毒感染胰腺β细胞并导致其HLA表达改变的能力。在整个培养期(6 - 8天)内均可分离到腮腺炎病毒,培养结束时,包括β细胞在内的60%的细胞含有病毒核衣壳蛋白。在一些受感染的培养物中观察到胰岛素分泌略有下降。感染总是与HLA I类分子表达增加相关。这种增强是由受感染细胞分泌的可溶性因子介导的。感染不能诱导HLA - DR分子的表达。然而,外源性干扰素 - γ能够使DR表达明显升高,且仅在非β细胞上观察到这种升高。风疹病毒和柯萨奇B4病毒也能够增强I类分子的表达,而单纯疱疹病毒2型则不能。结果表明,某些病毒能够感染β细胞并导致其免疫学外观改变。受感染胰岛中HLA I类表达增加可能通过增加自身反应性细胞毒性T细胞的活性而加剧糖尿病前期个体的自身免疫过程。