Objective: Human neutrophils express both activating and inhibitory Fcgamma receptors (FcgammaR), and their relative expression determines the inflammatory response to immune complexes. Tumor necrosis factor alpha (TNFalpha) up-regulates the expression of stimulatory FcgammaRIIa on neutrophils in vitro, and amplifies immune complex-induced activation of neutrophils in vivo. This study was undertaken to determine whether TNFalpha blockade in patients with rheumatoid arthritis (RA) alters the balance of activating FcgammaR and inhibitory FcgammaR and thereby decreases inflammation.
View Article and Find Full Text PDFJ Infus Nurs
January 2007
Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by an inflammation of the synovial membranes and progressive joint destruction, leading to significant impairment of physical function and quality of life. Rheumatoid arthritis imposes a substantial economic burden on both patients and society. The recent introduction of new biologic therapies for the treatment of RA reflects the application of knowledge obtained from advancements in the understanding of disease immunopathology.
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