title: Increased CD160 expression on circulating natural killer cells in atherogenesis.
abstract: BACKGROUND
  Atherosclerosis (AS) presents characteristic of a chronic inflammatory disease in which both adaptive and innate immune cells play roles. Accumulating evidence has showed the impairment of natural killer (NK) cells in atherosclerosis, however, the mechanisms of this impairment remain unclear. In this study, we investigated the expression of CD160 on NK cells and assessed its pathological roles in NK loss during atherogenesis.
  
  
  METHODS
  CD160 expression on NK cells was measured in 49 AS patients and 41 healthy controls (HC) by flow cytometry, their inflammatory cytokine levels in sera were determined by ELSIA, and the effect of CD160 engagement on NK cells was evaluated by in vitro culture experiments.
  
  
  RESULTS
  Compared to HC, AS patients had a significantly increased CD160 expression on peripheral NK cells and concomitantly decreased peripheral NK cell number, and increased CD160 expression was positively related to the levels of serum lipids and IFN-γ, TNF-α and IL-6 inflammation cytokines, which all are risk factors for atherogenesis, and inversely correlated with peripheral NK cell number. Furthermore, engagement of CD160 receptor on NK cells from AS patients triggers a significantly increased production of inflammation cytokines and subsequent NK cell apoptosis, and blockade of TNF-α prevented the increased apoptosis of NK cells from AS patients after CD160 engagement, indicating a critical role of TNF-α in mediating NK cell loss by CD160 engagement.
  
  
  RESULTS
  Our results provide evidence that elevated CD160 expression on NK cells plays an important role in NK cell loss in atherosclerosis. The increased CD160 expression on NK cells might be used as an indicator for disease progression.
authors.affiliation: Department of Cardiology, Navy General Hospital of Chinese PLA, Beijing, 100863, China. jjzz0581@126.com.
authors.forename: Jin
authors.initials: J
authors.lastname: Zuo
authors.affiliation: Department of Cardiology, General Hospital of Chinese PLA, Beijing, 100853, China. shanzl09@yeah.net.
authors.forename: Zhaoliang
authors.initials: Z
authors.lastname: Shan
authors.affiliation: Department of Interventional Radiology, 302 Hospital of Chinese PLA, Beijing, 100039, China. zlin1984_ngh@163.com.
authors.forename: Lin
authors.initials: L
authors.lastname: Zhou
authors.affiliation: Center of Health Examination, Navy General Hospital of Chinese PLA, Beijing, 100048, China. yujian_che@yeah.net.
authors.forename: Jian
authors.initials: J
authors.lastname: Yu
authors.affiliation: Center of Health Examination, Navy General Hospital of Chinese PLA, Beijing, 100048, China. conks1986@126.com.
authors.forename: Xiaopeng
authors.initials: X
authors.lastname: Liu
authors.affiliation: Department of Cardiology, Navy General Hospital of Chinese PLA, Beijing, 100863, China. gaoyuan_dc012@163.com.
authors.forename: Yuan
authors.initials: Y
authors.lastname: Gao
mesh_terms: D015703:Antigens, CD / Q000097:blood*; D017209:Apoptosis; D050197:Atherosclerosis / Q000097:blood* / Q000276:immunology* / Q000473:pathology; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D002465:Cell Movement; D005260:Female; D058851:GPI-Linked Proteins / Q000097:blood; D006801:Humans; D007694:Killer Cells, Natural / Q000378:metabolism*; D018655:Lymphocyte Count; D008297:Male; D008875:Middle Aged; D011971:Receptors, Immunologic / Q000097:blood*; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis / Q000097:blood
chemical_list: D015703:Antigens, CD; C114505:CD160 protein, human; D058851:GPI-Linked Proteins; D011971:Receptors, Immunologic; D014409:Tumor Necrosis Factor-alpha