INDUCTION OF INTERCELLULAR-ADHESION MOLECULE-1 (CD54) ON ISOLATED MOUSE PANCREATIC BETA-CELLS BY INFLAMMATORY CYTOKINES

被引:28
作者
PRIETO, J
KAAYA, EE
JUNTTIBERGGREN, L
BERGGREN, PO
SANDLER, S
BIBERFELD, P
PATARROYO, M
机构
[1] KAROLINSKA HOSP, DEPT PATHOL, S-10401 STOCKHOLM 60, SWEDEN
[2] KAROLINSKA HOSP, DEPT ENDOCRINOL, S-10401 STOCKHOLM 60, SWEDEN
[3] UNIV UPPSALA, DEPT MED CELL BIOL, S-75105 UPPSALA, SWEDEN
来源
CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY | 1992年 / 65卷 / 03期
基金
英国医学研究理事会;
关键词
D O I
10.1016/0090-1229(92)90154-G
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Insulin-dependent diabetes mellitus (IDDM) results from a T cell-dependent autoimmune destruction of insulin-producing pancreatic β cells. In the present study, expression of adhesion molecule ICAM-1 (CD54) on pancreatic β cells was studied in normal, obese hyperglycemic (ob/ob), and nonobese diabetic (NOD) mice. Freshly isolated pancreatic β cells from ob/ob mice did not express ICAM-1, but treatment of the cells with IL-1-β, TNF-α, or INF-γ strongly induced its expression as measured by immunofluorescence flow cytometry. The cytokines acted in a dose- and time-dependent manner. Maximal induction by either cytokine occurred at 24 hr and thereafter expression decreased, except for INF-γ. Immunoprecipitation from IL-1-β-treated β cells demonstrated a cell-surface glycoprotein with an apparent molecular weight of 95 kDa. ICAM-1 expression was undetectable on pancreatic β cells of normal and ob/ob mice as measured by immunohistochemistry. In NOD mice at different ages (1 to 6 months) ICAM-1 was also undetectable on β cells, in contrast to the strong expression on infiltrating mononuclear cells. The present study indicates that mouse pancreatic β cells, under certain conditions, can express ICAM-1. © 1992.
引用
收藏
页码:247 / 253
页数:7
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