Increased soluble FcγRIIIaMϕ in plasma from patients with coronary artery diseases

Atherosclerosis is the underlying disease process in patients affected with coronary artery diseases (CAD). Macrophages play a major role in the development of vascular lesions in atherogenesis. The cells express Fcγ receptor type IIIa (FcγRIIIa: CD16) identical to that in natural killer cells (NK cells), but with a cell type-specific glycosylation. In contrast, neutrophils express FcγRIIIb. These FcγRIIIs are released from the cell surface on activation, and these soluble forms (sFcγRIII) are present in the plasma. We measured sFcγRIIIaMϕ in the plasma with a newly developed anti-FcγRIII mAb, MKGR14, which recognizes FcγRIIIaMϕ specifically. The level of sFcγRIIIaMϕ, as well as the level of sFcγRIIIa (sFcγRIIIaMϕ plus sFcγRIIIaNK) or the level of total sFcγRIII (sFcγRIIIa plus sFcγRIIIb), were significantly increased in patients with CAD, but not in patients with vasospastic angina (VSA) or intact coronary arteries, compared with age-matched healthy donors. The sFcγRIIIaMϕ level was related to the number of significantly affected coronary arteries, and positively correlated with LDL-cholesterol to HDL-cholesterol ratios, but negatively with HDL-cholesterol. No correlation among the levels of three sFcγRIIIs was observed in CAD patients, as well as in healthy donors. The macrophages are activated during the process of atherosclerosis, and sFcγRIIIaMϕ may serve as a novel marker for atherosclerosis.