Role of Cytokines in the Pathogenesis of Anemia of Chronic Disease in Rheumatoid Arthritis

ArticleinClinical Immunology 92(2):153-160 · September 1999with13 Reads
Impact Factor: 3.67 · DOI: 10.1006/clim.1999.4736


    The aim of our study was to evaluate the role of proinflammatory cytokines: tumor necrosis factor α (TNFα), interleukin-1β (IL-1β), and interleukin-6 (IL-6), as well as the possible contribution of interleukin-10 (IL-10) in anemia of chronic disease (ACD) of rheumatoid arthritis (RA) patients. We measured the serum levels of TNFα, IL-1β, and IL-6 in 105 anemic and 127 nonanemic RA patients. We also investigated the effects of the above cytokines on the development of burst-forming units–erythroid (BFUe) and colony-forming units–erythroid (CFUe) in bone marrow cultures. Anemic patients had significantly higher serum levels of TNFα, IL-1β, and IL-6 compared to nonanemics. Serum IL-10 levels were low and there was no significant difference in IL-10 concentrations between anemic and nonanemic patients. Proinflammatory cytokines inhibited proliferation of BFUe and CFUe. IL-10 did not decrease the erythroid colony growth. Proinflammatory cytokines may play a role in the pathogenesis of ACD in RA patients. Low levels of IL-10 possibly contribute to the development of ACD.