title: KILLER CELL IMMUNOGLOBULIN-LIKE RECEPTOR GENES AND THEIR HLA-C LIGANDS IN HASHIMOTO THYROIDITIS IN A CHINESE POPULATION.
abstract: OBJECTIVE
  Natural killer (NK) cells serve as primary immune surveillance and are partially regulated by combinations of killer immunoglobulin-like receptors (KIR) and their human leukocyte antigen-C (HLA-C) ligands. Alterations in NK cell activity have been associated with Hashimoto thyroiditis (HT). The aim of this study was to determine whether certain KIR/HLA-C genotype combinations play a role in HT pathogenesis.
  
  
  METHODS
  The present study enrolled 107 unrelated HT patients and 108 random healthy individuals in a case-control study. Blood was collected for DNA extraction; typing of KIR genes and HLA-C alleles was performed by polymerase chain reaction with sequence specific primers (PCR-SSP), followed by electrophoresis on agarose gels.
  
  
  RESULTS
  Among a panel of KIR2D/HLA-C genotype combinations, the frequency of KIR2DS2/HLA-C1 was significantly increased in HT patients compared to controls (33.64% vs. 12.96%, P<.001). To further analyze the precise genotype, we investigated inhibitory or activating KIR/HLA-C gene pairs when their corresponding activating or inhibitory KIR genes were absent in the 2 groups. Only the frequency of KIR2DS2(-)2DL2/3(+)HLA-C1(+) was significantly decreased in HT patients compared to controls (48.60% vs. 70.37%, P = .001).
  
  
  CONCLUSIONS
  Our data suggest that KIR2DS2/HLA-C1 may correlate with HT pathogenesis. On the contrary, the predominance of KIR2DL2/3/HLA-C1 in the absence of KIR2DS2 suggests a potential inhibitory role in HT pathogenesis. In conclusion, our findings may further elucidate the mechanisms underlying the pathogenesis of HT and other autoimmune diseases.
  
  
  BACKGROUND
  HLA-C = human leukocyte antigen-C HT = Hashimoto thyroiditis KIR = killer immunoglobulin-like receptor NK = natural killer PCR = polymerase chain reaction.
authors.forename: Jian-Ting
authors.initials: JT
authors.lastname: Li
authors.forename: Cheng
authors.initials: C
authors.lastname: Guo
authors.forename: Ming-Long
authors.initials: ML
authors.lastname: Li
authors.forename: Yong-Qing
authors.initials: YQ
authors.lastname: Wei
authors.forename: Yan-Feng
authors.initials: YF
authors.lastname: Hou
authors.forename: Yu-Lian
authors.initials: YL
authors.lastname: Jiao
authors.forename: Yue-Ran
authors.initials: YR
authors.lastname: Zhao
authors.forename: Hui
authors.initials: H
authors.lastname: Sun
authors.forename: Jin
authors.initials: J
authors.lastname: Xu
authors.forename: Ming-Feng
authors.initials: MF
authors.lastname: Cao
authors.forename: Li
authors.initials: L
authors.lastname: Feng
authors.forename: Gui-Na
authors.initials: GN
authors.lastname: Yu
authors.forename: Ling
authors.initials: L
authors.lastname: Gao
authors.forename: Yi-Qing
authors.initials: YQ
authors.lastname: Liu
authors.forename: Bing-Chang
authors.initials: BC
authors.lastname: Zhang
authors.forename: Jia-Jun
authors.initials: JJ
authors.lastname: Zhao
authors.forename: Hai-Qing
authors.initials: HQ
authors.lastname: Zhang
mesh_terms: D000328:Adult; D044466:Asian People / Q000235:genetics; D016022:Case-Control Studies; D002681:China; D005260:Female; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease; D015236:HLA-C Antigens / Q000235:genetics*; D050031:Hashimoto Disease / Q000235:genetics* / Q000276:immunology; D006801:Humans; D008024:Ligands; D008297:Male; D008875:Middle Aged; D054340:Receptors, KIR / Q000235:genetics*
chemical_list: D015236:HLA-C Antigens; C433932:KIR2DS2 protein, human; C541358:KIR2DS3 protein, human; D008024:Ligands; D054340:Receptors, KIR