Increased soluble FcγRIIIa^M in plasma from patients with coronary artery diseases

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• 作者：Midori Masuda ; Hironori Miyoshi ; Shinzo Kobatake ; Noriko Nishimura ; Xian H. Dong ; Yutaka Komiyama and Hakuo Takahashi
• 刊名：Atherosclerosis
• 出版年：2006
• 出版时间：October 2006
• 年：2006
• 卷：188
• 期：2
• 页码：377-383
• 全文大小：251 K

文摘

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 sFcγRIIIa^M in the plasma with a newly developed anti-FcγRIII mAb, MKGR14, which recognizes FcγRIIIa^M specifically. The level of sFcγRIIIa^M, as well as the level of sFcγRIIIa (sFcγRIIIa^M plus sFcγRIIIa^NK) 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 sFcγRIIIa^M 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 sFcγRIIIa^M may serve as a novel marker for atherosclerosis.