Cross-linking of XXXX @entity4070 induces the production of granulocyte colony-stimulating factor and granulocyte-macrophage colony-stimulating factor by polymorphonuclear neutrophils.

@entity1 @entity4070 @entity1261 @entity589 @entity522 @entity4404 @entity12078 @entity1454 @entity4071 @entity1453 @entity9536 @entity2935 @entity2841
We have reported that @entity1 autoantibodies reacting with the polymorphonuclear neutrophil (PMN)-anchored @entity4070 ( @entity4071 ) protect these cells from spontaneous apoptosis. In this study, we used anti- @entity4071 F(ab')(2) to delineate the mechanism(s) whereby the PMN life span is extended. As documented using four methods, @entity4071 cross-linking impeded spontaneous apoptosis, whereas anti- @entity1454 F(ab')(2) exerted no effect. Incubation of PMNs with anti- @entity4071 prevented the up-regulation of @entity12078 integrins, particularly @entity9536 , which is the alpha-chain of complement receptor type 3, but also @entity1454 , which is its beta-chain, as well as @entity1453 and @entity2935 . Anti- @entity4071 -conditioned supernatant of PMNs diminished the percentage of @entity4404 -binding fresh PMNs after another 18 h in culture, whereas the negative control anti- @entity1454 had no effect. The expression of mRNA for @entity1261 and @entity2841 was induced by anti- @entity4071 , followed by the release of @entity1261 and @entity2841 in a dose-dependent manner. Anti- @entity1261 and anti- @entity2841 mAbs abrogated the antiapoptotic effect of the related growth factors. The delay in apoptosis was accompanied by a down-regulated expression of @entity589 , and a partial reduction of @entity522 activity. These data suggest an autocrine involvement of anti- @entity4071 -induced survival factors in the rescue of PMNs from spontaneous apoptosis. Thus, apoptosis of aged PMNs can be modulated by signaling through @entity4070 , which may occur in @entity1 with PMN-binding anti- @entity4070 autoantibodies.
