The Journal of Experimental Medicine
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Published online 2 April 2001.
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© The Rockefeller University Press, 0022-1007/2001/4/785/ $5.00
The Journal of Experimental Medicine, Volume 193, Number 7, April 2, 2001 785-792

Original Article

Inhibition of T1/St2 during Respiratory Syncytial Virus Infection Prevents T Helper Cell Type 2 (Th2)- but Not Th1-Driven Immunopathology

Gerhard Walzla, Stephen Matthewsa, Sharon Kendalla, Jose Carlos Gutierrez-Ramosb, Anthony J. Coyleb, Peter J.M. Openshawa, and Tracy Hussella

a Department of Respiratory Medicine, National Heart and Lung Institute at St. Mary's Hospital, Imperial College of Science, Technology and Medicine, London W2 1PG, United Kingdom
b Department of Biology, Inflammation Division, Millennium Pharmaceuticals, Incorporated, Cambridge, Massachusetts 02139
Department of Respiratory Medicine, National Heart and Lung Institute at St. Mary's, Imperial College School of Medicine, Norfolk Place, London W2 1PG, UK.44-0-20-7-262-891344-0-20-7-594-3853

p.openshaw{at}ic.ac.uk

T cells secreting interleukin (IL)-4 and IL-5 (T helper cell type 2 [Th2] cells) play a detrimental role in a variety of diseases, but specific methods of regulating their activity remain elusive. T1/ST2 is a surface ligand of the IL-1 receptor family, expressed on Th2- but not on interferon (IFN)-{gamma}–producing Th1 cells. Prior exposure of BALB/c mice to the attachment (G) or fusion (F) protein of respiratory syncytial virus (RSV) increases illness severity during intranasal RSV challenge, due to Th2-driven lung eosinophilia and exuberant Th1-driven pulmonary infiltration, respectively. We used these polar models of viral illness to study the recruitment of T1/ST2 cells to the lung and to test the effects of anti-T1/ST2 treatment in vivo. T1/ST2 was present on a subset of CD4+ cells from mice with eosinophilic lung disease. Monoclonal anti-T1/ST2 treatment reduced lung inflammation and the severity of illness in mice with Th2 (but not Th1) immunopathology. These results show that inhibition of T1/ST2 has a specific effect on virally induced Th2 responses and suggests that therapy targeted at this receptor might be of value in treating Th2-driven illness.

Key Words: bronchiolitis, viral • immunity, mucosal • immunity, cellular • pulmonary infection • eosinophil

Abbreviations used in this paper: BAL, bronchoalveolar lavage; RSV, respiratory syncytial virus.

Gerhard Walzl and Tracy Hussell's present address is Centre for Molecular Microbiology and Infection, Department of Biochemistry, Imperial College of Science, Technology and Medicine, London SW7 2AZ, UK.

© 2001 The Rockefeller University Press


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