ENHANCED METABOLISM OF ARACHIDONIC-ACID BY MACROPHAGES FROM NONOBESE DIABETIC (NOD) MICE

被引：24

作者：

LETY, MA ^{[1
]}

COULAUD, J ^{[1
]}

BENS, M ^{[1
]}

DARDENNE, M ^{[1
]}

HOMODELARCHE, F ^{[1
]}

机构：

[1] HOP TENON, INSERM, U64, F-75970 PARIS 20, FRANCE

来源：

CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY | 1992年 / 64卷 / 03期

关键词：

D O I：

10.1016/0090-1229(92)90199-X

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

The inbred nonobese diabetic (NOD) mouse spontaneously develops an autoimmune diabetes, which is now recognized as an experimental model for human type I insulin-dependent diabetes mellitus (IDDM). The autoimmune reaction, specifically directed against pancreatic β cells (insulitis), involves both macrophages and T lymphocytes. The study of the production of cyclooxygenase and lipoxygenase derivatives of arachidonic acid metabolism shows that in some conditions, and in particular in the presence of zymosan A, macrophages from NOD mice produced significantly more 6-keto-prostaglandin F1α (6-keto-PGF1α) and leukotriene C4 (LTC4) than macrophages from age- and sex-matched C57BL 6 mice. Moreover, zymosan A-stimulated macrophages from NOD females produced significantly more LTC4 than did macrophages from NOD males. These results may be of interest, given the bidirectional relationship between the various cytokines involved in the destruction of β cells of the islets of Langerhans and different eicosanoids. © 1992.

引用

页码：188 / 196

页数：9

共 83 条

[31] MACROPHAGE INFILTRATION PRECEDES AND IS A PREREQUISITE FOR LYMPHOCYTIC INSULITIS IN PANCREATIC-ISLETS OF PRE-DIABETIC BB RATS [J].