title: H2-EB1 Molecule Alleviates Allergic Rhinitis Symptoms of H2-Eb1 Knockout Mice.
abstract: BACKGROUND
  H2-EB1 molecule which is the homolog of Human HLA-DRB1 is proposed to be associated with allergic rhinitis (AR). Construction of H2-Eb1 knockout animal models provides a tool to elucidate the role of H2-EB1 and AR pathogenesis.
  
  
  OBJECTIVE
  To establish the H2-Eb1 knockout model and investigate the H2-EB1 functions in H2-Eb1 knockout mice as a model of AR.
  
  
  METHODS
  The Cre/LoxP system and ES gene knockout technology were applied to create heterozygous H2-Eb1 (+/-) knockout mice and their offspring of knockout homozygous(-/-), heterozygous (+/-) and wild type (+/+) H2-Eb1 mice. After identification, offspring of heterozygous (+/-) and homozygous (-/-) H2-Eb1 knockout mice were randomly selected to establish AR models to demonstrate the role of H2-Eb1 in AR pathogenesis.
  
  
  RESULTS
  The H2-Eb1 knockout mice model was successfully established. The reproduction and feeding of the homozygous (-/-) H2-Eb1 knockout mice were successful. Compared with the control group, the serum OVA-IgE and IL-4 levels significantly increased, while IFN-γ levels significantly dropped (p<0.05) in the experimental groups. For the two experimental groups, the homozygous (-/-) mice group had lower serum OVA-IgE and IL-4 levels, and higher IFN-γ levels than their heterozygous (+/-) counterparts (p<0.05), concomitant with slighter allergic symptoms (gentle behavior and less eosinophils in nasal mucosa).
  
  
  CONCLUSIONS
  Our study demonstrated that knockout of H2-Eb1 gene could alleviate mouse AR Symptoms, indicating H2-Eb1 may play an important role in regulating Th1/Th2 balance during the pathogenesis of AR.
authors.affiliation: Department of Otorhinolaryngology, the First Affiliated Hospital, Xinjiang Medical University, Urumqi, Xinjiang, China.
authors.forename: Linge
authors.initials: L
authors.lastname: Li
authors.forename: Bin
authors.initials: B
authors.lastname: Hu
authors.forename: Juan
authors.initials: J
authors.lastname: Feng
authors.forename: Yu
authors.initials: Y
authors.lastname: Zhang
authors.forename: Xi
authors.initials: X
authors.lastname: Shou
authors.forename: Yu
authors.initials: Y
authors.lastname: Tian
authors.forename: Chunrong
authors.initials: C
authors.lastname: Jiang
authors.forename: Hua
authors.initials: H
authors.lastname: Zhang
mesh_terms: D000485:Allergens / Q000276:immunology; D000818:Animals; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D004804:Eosinophils / Q000276:immunology*; D005260:Female; D059811:HLA-DRB1 Chains / Q000235:genetics; D000949:Histocompatibility Antigens Class II / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D007073:Immunoglobulin E / Q000097:blood; D007371:Interferon-gamma / Q000097:blood; D015847:Interleukin-4 / Q000097:blood; D008297:Male; D051379:Mice; D057507:Mice, 129 Strain; D018345:Mice, Knockout; D009297:Nasal Mucosa / Q000473:pathology*; D010047:Ovalbumin / Q000276:immunology; D065631:Rhinitis, Allergic / Q000276:immunology*; D058408:Th1-Th2 Balance; D018418:Th2 Cells / Q000276:immunology*
chemical_list: D000485:Allergens; D016207:Cytokines; D059811:HLA-DRB1 Chains; D000949:Histocompatibility Antigens Class II; C024138:I-E-antigen; D015847:Interleukin-4; D007073:Immunoglobulin E; D007371:Interferon-gamma; D010047:Ovalbumin