摘要:

Recombinant Interleukin-1β(rIL-1β) induced dose-dependent synthesis of PGE2and activation of both cell-associated and soluble phospholipase A2(PLA2) in cultured mouse peritoneal macrophages. Kinetic studies showed that rIL-1βwas able to induce a 2-fold increase in membrane bound PLA2activity in the cells within 1 hour. Elevated levels of PGE2were however observed only after 4 hours stimulation of the cells while significant levels of soluble PLA2activity were observed only after 16 hours stimulation of the cells. Stimulation with rIL-1βof macrophage cultures pre-labelled with [l4C]arachidonic acid resulted in a loss of label from both phosphatidyl-choline and phosphatidylinositol in only 10min. which was not observed in control (unstimulated) cultures. These results are indicative that the two phospholipids are the principal source of arachidonic acid for IL-1 induced prostaglandin synthesis.

ISSN:0891-6934    

DOI:10.3109/08916939008998435

出版商:Taylor&Francis    

年代:1990

数据来源: Taylor

摘要:

The aim of this work was to study possible differences in the humoral response against autologous and heterologous (bacterial and mammalian) ssDNA in children with diffuse connective tissue diseases (DCTD) compared with age matched controls. We found that IgM anti ssDNA were significantly increased in systemic lupus eritematosus (SLE) and in juvenile arthritis (JA), but not in juvenile dermatomyositis (JDM). IgG anti ssDNA were significantly elevated only in children with SLE. We next evaluated the binding specificity to human and bacterial ssDNA by inhibition assays. We found that SLE and JA sera recognised epitopes shared in common to endogenous and bacterial ssDNA. In contrast, in normal subjects IgG binding to bacterial DNA was not inhibited by human DNA, while IgG anti human ssDNA were cross reactive with the bacterial antigen.These data suggest that natural antibodies (IgM) producing cells are activated in some but not all DCTD, and that normal children have different reactivity against autologous and heterologous ssDNA with respect to SLE and JA patients.

ISSN:0891-6934    

DOI:10.3109/08916939008998436

出版商:Taylor&Francis    

年代:1990

数据来源: Taylor

ISSN:0891-6934    

DOI:10.3109/08916939008998437

出版商:Taylor&Francis    

年代:1990

数据来源: Taylor

ISSN:0891-6934    

DOI:10.3109/08916939008998438

出版商:Taylor&Francis    

年代:1990

数据来源: Taylor