Increased Expression of Fc-γ Receptors on Monocytes in Patients With Nascent Metabolic Syndrome

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The metabolic syndrome (MetS) confers an increased propensity for diabetes and cardiovascular disease. C-reactive protein (CRP) levels are increased in MetS and predict cardiovascular events. Fc-γ receptors (FcgRs) are immune receptors on macrophages and include FcgRI (CD64), FcgRII (CD32), and FcgRIII (CD16).


CRP has been shown to be processed by CD32 and CD64 in human monocytes. Although MetS is characterized by increased CRP and monocyte proinflammatory activity, data on FcgR expression on monocytes in patients with MetS compared with those of control subjects are sparse. Thus, the aim of the study was to examine this expression and the correlation with CRP.

Design and Setting:

After informed consent was given, patients with MetS (n = 50) and control subjects (n = 40) were studied. CD32 and CD64 expression on monocytes was examined by both flow cytometry and Western blotting. Immunoprecipitation studies were performed to examine spleen tyrosine kinase (Syk) activity as a measure of CD32 and CD64 activity.


Surface expression of CD32 and CD64 was significantly increased in patients with MetS compared with that in control subjects even after adjustment for body mass index and waist circumference. Expression of these FcgRs increased significantly with the number of features of MetS (Ptrend < .001) and correlated with levels of high-sensitivity CRP (P < .01). CRP after engagement of CD32 and CD64 signals via Syk. Syk phosphorylation was increased in monocytes of patients with MetS compared with that in control subjects.


We provide novel evidence of increased FcgR expression and activity in monocytes of patients with MetS that correlates with the number of features of MetS and with high-sensitivity CRP.

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