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IL‐33 Receptor (ST2) Signalling is Important for Regulation of Th2‐Mediated Airway Inflammation in a Murine Model of Acute Respiratory Syncytial Virus Infection
Author(s) -
Zeng S.,
Wu J.,
Liu J.,
Qi F.,
Liu B.
Publication year - 2015
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/sji.12284
Subject(s) - immunology , cytokine , inflammation , immune system , receptor , biology , eosinophil , monoclonal antibody , antibody , asthma , biochemistry
T1/ ST 2, 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 T h2 cell‐dominant immune responses. The function of IL ‐33/ ST 2 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 ST 2 mRNA as well as a massive infiltration of CD 45 + ST 2 + cells in the lungs, suggesting that during the early phase of RSV infection, IL ‐33 target cells which express ST 2 on cell surface, may play a critical role for the development of RSV ‐induced airway inflammation. Indeed, blocking ST 2 signalling using anti‐ ST 2 monoclonal antibody diminished not only RSV ‐induced eosinophil recruitment, but also the amounts of T h2‐associated cytokines, particularly IL ‐13, and T h17‐type cytokine IL ‐17 A in the lungs of infected mice. However, anti‐ ST 2 antibody treatment did not affect the production of T h1‐type cytokine IFN ‐ γ as well as pulmonary viral growth and clearance. These results indicate that IL ‐33/ ST 2 signalling is involved in RSV ‐induced, T h2‐associated airway inflammation but not protective immunity.