title: Respiratory syncytial virus protects against the subsequent development of ovalbumin-induced allergic responses by inhibiting Th2-type γδ T cells.
abstract: Respiratory syncytial virus (RSV) infection has been hypothesized to be a risk factor for the development of allergy and asthma, but epidemiologic studies in humans still remain inconclusive. The association between RSV infection and allergic diseases may be dependent on an atopic background and previous history of RSV infection. It has been reported that RSV infection before sensitization to an allergen decreased the production of Th2-like cytokines in the lung and the levels of allergen-specific Th2-type antibodies in the serum. However, the underlying mechanisms are largely unknown. In the present study, the role of pulmonary γδ T cells in RSV-affected, allergen-induced airway inflammation was investigated. BALB/c mice were sensitized to or challenged with ovalbumin (OVA) and infected with RSV either before or after the sensitization period. It became clear that sensitization and challenge of mice with OVA induced a large influx of γδ T cells to the lungs. However, prior RSV infection inhibited the infiltration of γδ T cells as well as activated γδ T cells, characterized by expression of CD40L or CD69 molecular in the cell surface. Moreover, prior RSV infection elevated the type 1 cytokine gene expression but suppressed type 2 cytokine expression in the lung γδ T cells. Adoptive transfer of γδ T cells from OVA-sensitized and challenged mice increased airway inflammation, suggesting that γδ T cells may play a proinflammatory role in allergic responses. These results described here support the idea of an unknown γδ T cell-dependent mechanism in the regulation of RSV-affected, allergen-induced allergic airway responses.
authors.affiliation: Department of Immunology, School of Basic Medical Science, China Medical University, Shenyang, China.
authors.forename: Leiying
authors.initials: L
authors.lastname: Zhang
authors.forename: Jing
authors.initials: J
authors.lastname: Liu
authors.forename: Enhua
authors.initials: E
authors.lastname: Wang
authors.forename: Bing
authors.initials: B
authors.lastname: Wang
authors.forename: Sheng
authors.initials: S
authors.lastname: Zeng
authors.forename: Jianqi
authors.initials: J
authors.lastname: Wu
authors.forename: Yoshinobu
authors.initials: Y
authors.lastname: Kimura
authors.forename: Beixing
authors.initials: B
authors.lastname: Liu
mesh_terms: D000818:Animals; D015703:Antigens, CD / Q000032:analysis; D000945:Antigens, Differentiation, T-Lymphocyte / Q000032:analysis; D023201:CD40 Ligand / Q000032:analysis; D016207:Cytokines / Q000096:biosynthesis; D005260:Female; D020869:Gene Expression Profiling; D006967:Hypersensitivity / Q000276:immunology*; D007108:Immune Tolerance; D037181:Lectins, C-Type / Q000032:analysis; D051379:Mice; D008807:Mice, Inbred BALB C; D016692:Receptors, Antigen, T-Cell, gamma-delta / Q000032:analysis / Q000276:immunology*; D012136:Respiratory Syncytial Viruses / Q000276:immunology / Q000472:pathogenicity*; D015843:Serpins / Q000276:immunology*; D016176:T-Lymphocyte Subsets / Q000737:chemistry / Q000276:immunology; D018418:Th2 Cells / Q000737:chemistry / Q000276:immunology*; D000099192:CD69 Antigens
chemical_list: D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D023201:CD40 Ligand; D016207:Cytokines; D037181:Lectins, C-Type; D016692:Receptors, Antigen, T-Cell, gamma-delta; D015843:Serpins; D000099192:CD69 Antigens; C085344:SERPIN-B5