Production of @entity1356 , @entity1193 and @entity688 by blood mononuclear cells in chronic XXXX .

@entity1 @entity625 @entity1356 @entity5 @entity39 @entity1193 @entity688 @entity309 @entity617
Joint erosion is a prevalent feature of @entity309 ( @entity309 ) but not of many other chronic inflammatory arthritides (non- @entity309 ). Joint destruction is mediated by cytokines, primarily interleukin (IL)-1 and @entity5 @entity39 factor. Less erosive activity in @entity1 with non- @entity309 compared to @entity309 might be related to factors that inhibit production and/or function of IL-1. Release of @entity1356 , and the two antagonists, @entity1193 ( @entity1193 ) and @entity688 from blood mononuclear cells were therefore quantitated by ELISA in 22 @entity1 with @entity309 , 11 with non- @entity309 and 15 healthy age-matched controls. Release of @entity1356 was comparable between the three groups but only detectable in cultures stimulated with lipopolysaccharide; it decreased in @entity1 treated with @entity617 : 3.8 ng/10(6)monocytes (median) vs 11.7 (P=0.045). Release of @entity1193 was in all but IgG-stimulated cultures comparable between groups. The ratio of @entity1193 / @entity1356 was elevated in LPS-stimulated cells from @entity309 @entity1 only: 2.0 versus 1.3 (P=0.02). In contrast, IgG-induced @entity1193 release was significantly elevated only in non- @entity309 @entity1 : 95 ng/10(6)monocytes vs 40 (P=0.014), and the levels correlated positively to those of blood CRP (P=0.02). Though stimulated release of @entity688 was similar between the three groups, the levels were lower in @entity625 @entity1 , and controls (P=0. 05). In conclusion, increased IgG-stimulated @entity1193 release and elevated @entity1193 / @entity1356 ratio may protect against actions of IL-1 in vivo, and decreased release of @entity688 might be related to features of @entity625 .
