Changes of dendritic cells and fractalkine in type 2 diabetic patients with unstable angina pectoris: a preliminary reportReport as inadecuate




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Cardiovascular Diabetology

, 10:50

First Online: 10 June 2011Received: 21 April 2011Accepted: 10 June 2011

Abstract

BackgroundIt has been shown that dendritic cells DCs and fractalkine play a role in accelerating progression of the inflamed atherosclerotic lesions and plaque rupture. We evaluated the numbers and functional changes of DCs and its subsets in human type 2 diabetes with or without unstable angina pectoris UAP.

MethodsThe study population consisted of 39 diabetic patients DM:18 without CAD; DM + UAP: 21 with UAP, 18 non-diabetic UAP patients UAP, and 15 healthy control Normal. Peripheral blood DCs and its subsets were measured by three color flow cytometry. Serum levels of fractalkine, IL-12, and IFN-α were also measured. The functional status of the monocyte-derived DCs was analyzed by flow cytometry and allogeneic mixed T lymphocytes reaction.

ResultsThe percent and absolute numbers of DCs and mDC within the total leukocyte population was similar for Normal and DM, while significantly lower in DM + UAP. pDC numbers were not significantly altered. Serum fractalkine in DM + UAP was highest among the four groups p = 0.04 vs. UAP, p = 0.0003 vs. DM, p < 0.0001 vs. Normal. Circulating mDC inversely correlated with serum fractalkine r = -0.268, p = 0.01 level. Compared with DM and UAP, the costimulatory molecules CD86 and proliferation of T cells stimulated by DCs were significantly increased in DM + UAP group.

ConclusionsOur study suggested that increases in the fractalkine level and the number and functional changes of blood DCs might contribute to diabetic coronary atherosclerosis and plaque destabilization.

Keywordsdendritic cell fractalkine unstable angina pectoris type 2 diabetes atherosclerosis immune response AbbreviationsCADcoronary artery disease

APCsantigen-presenting cells

DCsdendritic cells

mDCmysloid dendritic cell

pDCplasmacytoid dendritic cell

sFKNserum fractalkine

UAPunstable angina pectoris

DMdiabetes mellitus

AGEsadvanced glycosylation end products

MLRmixed T lymphocytes reaction

FITCfluorescein isothiocyanate

FSC-Hforward scatter

PEphycoerythrin

IgGimmunoglobulin G

GM-CSFgranulocyte-macrophage colony-stimulating factor

IL-4interleukin-4

IL-12interleukin-12

IFN-αinterferon-alpha

CX3CR1C-X3-C motif receptor 1.

Electronic supplementary materialThe online version of this article doi:10.1186-1475-2840-10-50 contains supplementary material, which is available to authorized users.

Kang Yao, Hao Lu contributed equally to this work.

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Author: Kang Yao - Hao Lu - Rongchong Huang - Shuning Zhang - Xiaowu Hong - Hongyu Shi - Aijun Sun - Juying Qian - Yunzeng Zou -

Source: https://link.springer.com/article/10.1186/1475-2840-10-50







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