Infection with respiratory syncytial virus influences FasL-mediated apoptosis of pulmonary γδ T cells in a murine model of allergen sensitization. (May 2014)

• Record Type: Journal Article
• Authors: Zeng, Sheng; Wu, Jianqi; Liu, Jing; Qi, Feifei; Kimura, Yoshinobu; Cao, Yaming; Liu, Beixing
• Is Part Of: Journal of asthma. Volume 51:Number 4(2014)
• Page Start: 360
• Page End: 365
• Publication Date: 2014-05
• Subjects: Asthma -- Periodicals; 616.238005
• DOI: 10.3109/02770903.2013.878954
• Languages: English
• ISSNs: 0277-0903

Abstract

<abstract> <title>Abstract</title> <p> <italic>Background</italic>: 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. <italic>Methods</italic>: 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. <italic>Results</italic>: 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. <italic>Conclusions</italic>: 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.</p> </abstract>