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DOI 10.1016/j.jdiacomp.2018.11.004

Медицинская библиотека · Journal of diabetes and its complications · 2018

Dendritic cell activation is blunted in patients with coronary artery disease and diabetes mellitus.

Yetkin Gulay Imadoglu, Yucel Aysegul Atak, Tekin İshak Özel, Yılmaz Mustafa, Atalay Hakan, Yetkin Ertan

СтатьяПоддержка исследования: вне правительства СШАПеревод пока не подготовлен

Аннотация

BACKGROUND

It has been shown that functional status of dendritic cells (DCs) in diabetic patients with unstable angina pectoris (UAP) are more mature and activated than diabetic patients without coronary artery disease (CAD) and none diabetic patients with UAP. Accordingly we aimed to assess the activation of DCs in patients with CAD with/and without Diabetes Mellitus (DM) and compare to those in subjects with normal coronary arteries (NCA).

MATERIALS AND

METHODS

Twenty three patients with severe CAD who were scheduled to coronary artery by-pass grafting surgery and 6 patients with angiographycally NCAs were included in the study. Activation of peripheral blood DCs have been analyzed by flow cytometric measures of CD86 activation.

RESULTS

In patients with CAD and without DM, DC activation significantly increased after stimulation of oxidesized LDL (135 ± 121 vs 248 ± 197 p = 0.024). However this activation didn't significantly increased in patients with CAD and DM (100 ± 20 vs 120 ± 97, p = 0,54). Patients with NCAs and without DM showed marked activation of CD86 after stimulation with ox-LDL.

CONCLUSION

We have documented that DC activation, upon stimulation of ox-LDL has blunted in patients with CAD compared to patients with NCAs. Moreover this defective activation is more pronounced in those with diabetic patients with CAD.

Для цитирования: Yetkin Gulay Imadoglu, Yucel Aysegul Atak, Tekin İshak Özel, Yılmaz Mustafa, Atalay Hakan, Yetkin Ertan. Dendritic cell activation is blunted in patients with coronary artery disease and diabetes mellitus.. Journal of diabetes and its complications. 2018. DOI: 10.1016/j.jdiacomp.2018.11.004.

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