Key result
Acute MI linked to ~64% lower circulating myeloid dendritic cell precursors vs healthy controls.
Why the study?
Circulating dendritic cell precursors are reduced in several autoimmune diseases, and atherosclerosis has autoimmune features, but their frequency in CAD and atherosclerotic plaques was unclear.
Are circulating myeloid and plasmacytoid dendritic cell precursors altered in patients with coronary artery disease and in vulnerable atherosclerotic plaques?
Cross-Sectional (n=140)
Are circulating myeloid and plasmacytoid dendritic cell precursors altered in patients with coronary artery disease and in vulnerable atherosclerotic plaques?
The reduction of circulating mDC precursors in CAD patients and their accumulation in vulnerable plaques suggest that these cells are actively recruited into atheromata, supporting the concept of atherosclerosis as an autoimmune-like process.
OBJECTIVES: We analyzed the frequency of myeloid dendritic cell (mDC) and plasmacytoid dendritic cell (pDC) precursors in blood of patients with coronary artery disease (CAD) and in atherosclerotic carotid plaques of patients with cerebrovascular disease (CVD). BACKGROUND: Circulating DC precursors are reduced in several autoimmune diseases. Atherosclerosis has features of an autoimmune disease, such as the presence of autoantibodies or autoreactive T cells. Tissue-resident DCs were previously described in atheromata, and it is assumed that they are important for the activation of T cells against autoantigens there. METHODS: Circulating mDC and pDC precursors were flow cytometrically detected in healthy controls (n = 19), CAD patients with stable (n = 20) and unstable angina pectoris (n = 19), and acute myocardial infarction (n = 17). In human carotid plaques (n = 65), mDC and pDC precursors were identified immunohistochemically. RESULTS: Circulating mDC precursors were significantly reduced in patients with stable angina pectoris (0.19%, p = 0.04), unstable angina pectoris (0.16%, p = 0.004), and acute myocardial infarction (0.08%, p < 0.001) compared with control patients (0.22% of peripheral blood mononuclear cells). In contrast, pDC numbers were not significantly altered. Circulating mDC precursors inversely correlated with high-sensitivity C-reactive protein (r = -0.38, p = 0.001) or interleukin-6 (r = -0.42, p < 0.001). In contrast to pDC, significantly more mDC precursors were observed in vulnerable carotid plaques (24, 0.25 mm2; n = 31; p = 0.003) than in stable ones (6.4, 0.25 mm2; n = 34). CONCLUSIONS: Similar to autoimmune diseases, circulating mDC precursors were significantly reduced in patients with CAD. The emergence of mDC precursors in vulnerable plaques suggests their recruitment into atheromata as a possible reason for their decrease in blood. In contrast, no significant association of circulating pDC precursors with atherosclerosis was observed.
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Yılmaz et al. (2006) conducted a cross-sectional in Coronary artery disease and cerebrovascular disease (n=140). Coronary artery disease (stable angina, unstable angina, acute myocardial infarction) vs. Healthy controls was evaluated on Frequency of circulating myeloid dendritic cell (mDC) precursors (p=<0.001). Circulating myeloid dendritic cell precursors were significantly reduced in patients with acute myocardial infarction (0.08%, P<0.001) and angina compared with healthy controls (0.22%).
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