title: Changes of dendritic cells and fractalkine in type 2 diabetic patients with unstable angina pectoris: a preliminary report.
abstract: BACKGROUND
  It 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).
  
  
  METHODS
  The 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.
  
  
  RESULTS
  The 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.
  
  
  CONCLUSIONS
  Our 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.
authors.affiliation: Department of Cardiology, Zhongshan Hospital, Shanghai Institute of Cardiovascular Diseases, 180 Fenglin Road, Shanghai, China.
authors.forename: Kang
authors.initials: K
authors.lastname: Yao
authors.forename: Hao
authors.initials: H
authors.lastname: Lu
authors.forename: Rongchong
authors.initials: R
authors.lastname: Huang
authors.forename: Shuning
authors.initials: S
authors.lastname: Zhang
authors.forename: Xiaowu
authors.initials: X
authors.lastname: Hong
authors.forename: Hongyu
authors.initials: H
authors.lastname: Shi
authors.forename: Aijun
authors.initials: A
authors.lastname: Sun
authors.forename: Juying
authors.initials: J
authors.lastname: Qian
authors.forename: Yunzeng
authors.initials: Y
authors.lastname: Zou
authors.forename: Junbo
authors.initials: J
authors.lastname: Ge
mesh_terms: D000328:Adult; D000368:Aged; D000789:Angina, Unstable / Q000097:blood* / Q000453:epidemiology / Q000473:pathology*; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D049109:Cell Proliferation; D054428:Chemokine CX3CL1 / Q000097:blood*; D015897:Comorbidity; D003324:Coronary Artery Disease / Q000503:physiopathology; D003713:Dendritic Cells / Q000473:pathology*; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000453:epidemiology / Q000473:pathology*; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D016898:Interferon-alpha / Q000097:blood; D018664:Interleukin-12 / Q000097:blood; D008297:Male; D008875:Middle Aged; D058226:Plaque, Atherosclerotic / Q000503:physiopathology; D013601:T-Lymphocytes / Q000473:pathology
chemical_list: D015415:Biomarkers; D054428:Chemokine CX3CL1; D016898:Interferon-alpha; D018664:Interleukin-12