February 28, 2017
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CD14brightCD16+ monocytes correlated with RA disease activity

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The proportion of CD14brightCD16+ monocytes was positively associated with disease activity in patients with rheumatoid arthritis and was induced by the cytokine interleukin-10, according to recently published data.

“In this study, we demonstrate that circulating CD14brightCD16+ monocytes are increased in patients with [rheumatoid arthritis] RA in the active phase and decrease after [methotrexate] MTX treatment in a manner that correlates with decreasing disease activity,” Tsuotomu Takeuchi, MD, PhD, in the Division of Rheumatology of the Department of Internal Medicine at Keio University School of Medicine in Japan, and colleagues wrote. “Moreover, this monocyte subset is associated with expression of inflammatory cytokines in peripheral blood, and the cytokine [interleukin-10] IL-10, which is increased in patients with RA, induces CD16 expression on monocytes.”

Takeuchi and colleagues used flow cytometry to assess three subsets of peripheral blood monocytes and measured serum cytokines at baseline in 35 patients with RA and 14 healthy controls. Researchers isolated CD14brightCD16- monocytes and cultured in vitro with different cytokines for 14 hours and assessed CD16 induction.

Researchers found the proportion of CD14brightCD16+ monocytes, as well as serum IL-6, IL-8 and IL-10, increased in patients with RA compared with healthy controls. The proportion of CD14brightCD16+ monocytes positively correlated with RA disease activity; whereas, the proportion of CD14brightCD16- monocytes negatively correlated with disease activity. Researchers found isolated CD14brightCD16- monocytes were stimulated with IL-6, IL-8 and IL-10; however, the only cytokine to significantly induce CD16 expression was IL-10.

“These results suggest that CD14brightCD16+ monocytes play a role in the pathogenesis of RA, and that IL-10 is a key cytokine in the regulation of CD16 expression,” the researchers wrote. – by Will Offit

 

Disclosures: Researchers report the work was supported by an institutional research grant from Keio University. Takeuchi reports lecture fees or research grants from Abbot Japan Co., Ltd., Astellas Pharma, Bristol-Myers K.K., Chugai Pharmaceutical Co. Ltd., Daiichi Sankyo Co. Ltd., Eisai Co. Ltd., Janssen Pharmaceutical K.K., Mitsubishi Tanabe Pharma Co., Pfizer Japan Inc., Sanofi-Aventis K.K., Santen Pharmaceutical Co. Ltd., Teijin Pharma Ltd., Asahikasei Pharma Corp., Taisho Toyama Pharmaceutical Co. Ltd., Janssen Pharmaceutical K.K., Astra Zeneca K.K., Eli Lilly Japan K.K., Novartis Pharma K.K. and Abbvie GK. Please see the full study for a list of all other relevant financial disclosures.