title: Infection with respiratory syncytial virus influences FasL-mediated apoptosis of pulmonary γδ T cells in a murine model of allergen sensitization.
abstract: BACKGROUND
  It has been reported that adoptive transfer of γδ T cells increases the cellular infiltration, especially eosinophils, in the lungs of allergic mice, suggesting that γδ T cells may play a proinflammatory role in allergic airway inflammation. Respiratory syncytial virus (RSV) infection can decrease the number of Th2-type γδ T cells. However, the underlying mechanisms remain unknown.
  
  
  METHODS
  BALB/c mice were inoculated intranasally with RSV before or after sensitization to OVA. The amounts of Th1/Th2 cytokines as well as the levels of specific antibodies were determined by ELISA. The apoptotic death of pulmonary γδ T cells was analyzed by flow cytometry.
  
  
  RESULTS
  Adoptive transfer of γδ T cells increased the production of Th2 cytokines in the lungs and allergy-related antibodies in the serum, further confirming that γδ T cells act as pro-inflammatory cells or a promoter for the development of allergic asthma. RSV infection before sensitization to OVA enhanced apoptotic death of pulmonary γδ T cells. The percentage and absolute number of FasL-expressing γδ T cells in the lungs of allergic mice were elicited significantly by prior RSV infection. Blocking FasL with monoclonal antibody diminished apoptotic death of γδ T cells, suggesting that FasL is important for RSV-induced apoptosis of pulmonary γδ T cells.
  
  
  CONCLUSIONS
  This work provides evidence that RSV infection suppresses the subsequent development of OVA-induced allergic responses partly by enhancing FasL-mediated apoptosis of pulmonary γδ T cells.
authors.affiliation: Department of Immunology, School of Basic Medical Science, China Medical University , Shenyang , PR China .
authors.forename: Sheng
authors.initials: S
authors.lastname: Zeng
authors.forename: Jianqi
authors.initials: J
authors.lastname: Wu
authors.forename: Jing
authors.initials: J
authors.lastname: Liu
authors.forename: Feifei
authors.initials: F
authors.lastname: Qi
authors.forename: Yoshinobu
authors.initials: Y
authors.lastname: Kimura
authors.forename: Yaming
authors.initials: Y
authors.lastname: Cao
authors.forename: Beixing
authors.initials: B
authors.lastname: Liu
mesh_terms: D000485:Allergens; D000704:Analysis of Variance; D000818:Animals; D017209:Apoptosis / Q000276:immunology; D016207:Cytokines / Q000276:immunology / Q000378:metabolism; D004195:Disease Models, Animal; D053222:Fas Ligand Protein / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D005260:Female; D007114:Immunization; D051379:Mice; D008807:Mice, Inbred BALB C; D010047:Ovalbumin / Q000276:immunology / Q000494:pharmacology; D011014:Pneumonia / Q000276:immunology* / Q000503:physiopathology; D011897:Random Allocation; D012016:Reference Values; D018357:Respiratory Syncytial Virus Infections / Q000276:immunology* / Q000503:physiopathology; D012136:Respiratory Syncytial Viruses / Q000276:immunology* / Q000472:pathogenicity; D012141:Respiratory Tract Infections / Q000276:immunology / Q000503:physiopathology / Q000821:virology*; D018570:Risk Assessment; D012680:Sensitivity and Specificity; D018418:Th2 Cells / Q000276:immunology
chemical_list: D000485:Allergens; D016207:Cytokines; C505661:FASLG protein, human; D053222:Fas Ligand Protein; D010047:Ovalbumin