title: IL-33 Receptor (ST2) Signalling is Important for Regulation of Th2-Mediated Airway Inflammation in a Murine Model of Acute Respiratory Syncytial Virus Infection.
abstract: T1/ST2, an orphan receptor with homology with the interleukin (IL)-1 receptor family, is the ligand-binding component of the receptor for the cytokine IL-33, a newly identified cytokine known to amplify the Th2 cell-dominant immune responses. The function of IL-33/ST2 signalling during respiratory syncytial virus (RSV) infection is not fully known. In this study, following intranasal infection with RSV, BALB/c mice showed a marked increase in the production of IL-33, with an elevated expression of ST2 mRNA as well as a massive infiltration of CD45(+) ST2(+) cells in the lungs, suggesting that during the early phase of RSV infection, IL-33 target cells which express ST2 on cell surface, may play a critical role for the development of RSV-induced airway inflammation. Indeed, blocking ST2 signalling using anti-ST2 monoclonal antibody diminished not only RSV-induced eosinophil recruitment, but also the amounts of Th2-associated cytokines, particularly IL-13, and Th17-type cytokine IL-17A in the lungs of infected mice. However, anti-ST2 antibody treatment did not affect the production of Th1-type cytokine IFN-γ as well as pulmonary viral growth and clearance. These results indicate that IL-33/ST2 signalling is involved in RSV-induced, Th2-associated airway inflammation but not protective immunity.
authors.affiliation: Department of Immunology, School of Basic Medical Science, China Medical University, Shenyang, China.
authors.forename: S
authors.initials: S
authors.lastname: Zeng
authors.affiliation: Batch 2011 of Clinical Medicine, Harbin Medical University, Harbin, China.
authors.forename: J
authors.initials: J
authors.lastname: Wu
authors.affiliation: Department of Immunology, School of Basic Medical Science, China Medical University, Shenyang, China.
authors.forename: J
authors.initials: J
authors.lastname: Liu
authors.affiliation: Department of Immunology, School of Basic Medical Science, China Medical University, Shenyang, China.
authors.forename: F
authors.initials: F
authors.lastname: Qi
authors.affiliation: Department of Immunology, School of Basic Medical Science, China Medical University, Shenyang, China.
authors.forename: B
authors.initials: B
authors.lastname: Liu
mesh_terms: D000208:Acute Disease; D000818:Animals; D045744:Cell Line, Tumor; D016207:Cytokines / Q000276:immunology / Q000378:metabolism; D004195:Disease Models, Animal; D004797:Enzyme-Linked Immunosorbent Assay; D004804:Eosinophils / Q000276:immunology / Q000378:metabolism; D005260:Female; D015870:Gene Expression / Q000276:immunology; D054884:Host-Pathogen Interactions / Q000276:immunology; D006801:Humans; D007249:Inflammation / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D000072179:Interleukin-1 Receptor-Like 1 Protein; D000067596:Interleukin-33; D007378:Interleukins / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D017493:Leukocyte Common Antigens / Q000276:immunology / Q000378:metabolism; D008168:Lung / Q000276:immunology / Q000378:metabolism / Q000821:virology; D008807:Mice, Inbred BALB C; D018123:Receptors, Interleukin / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D018357:Respiratory Syncytial Virus Infections / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D012136:Respiratory Syncytial Viruses / Q000276:immunology / Q000502:physiology; D012137:Respiratory System / Q000276:immunology* / Q000473:pathology / Q000821:virology; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015398:Signal Transduction / Q000235:genetics / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology* / Q000378:metabolism
chemical_list: D016207:Cytokines; C486189:Il1rl1 protein, mouse; C506535:Il33 protein, mouse; D000072179:Interleukin-1 Receptor-Like 1 Protein; D000067596:Interleukin-33; D007378:Interleukins; D018123:Receptors, Interleukin; D017493:Leukocyte Common Antigens