The Journal of Experimental Medicine
Janeway's Immunobiology 7th Edition
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Published online 26 March 2001.
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*Respiratory Syncytial Virus Infections
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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

Correspondence to: Peter J.M. Openshaw, Department of Respiratory Medicine, National Heart and Lung Institute at St. Mary's, Imperial College School of Medicine, Norfolk Place, London W2 1PG, UK. Tel:44-0-20-7-594-3853 Fax:44-0-20-7-262-8913 E-mail: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


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