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Journal of Virology, March 2004, p. 3014-3023, Vol. 78, No. 6
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.6.3014-3023.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Treatment with Anti-LFA-1 Delays the CD8+ Cytotoxic-T-Lymphocyte Response and Viral Clearance in Mice with Primary Respiratory Syncytial Virus Infection

John A. Rutigliano,1,2 Teresa R. Johnson,1 Tonya N. Hollinger,3 Julie E. Fischer,2 Sandra Aung,2,{dagger} and Barney S. Graham1*

Vaccine Research Center, National Institutes of Health, Bethesda, Maryland 20892,1 Departments of Microbiology and Immunology,2 Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee 372323

Received 26 August 2003/ Accepted 12 November 2003

Cytotoxic T lymphocytes (CTLs) play an important role in the immune response against respiratory syncytial virus (RSV) infection. The cell surface molecule lymphocyte function-associated antigen 1 (LFA-1) is an important contributor to CTL activation, CTL-mediated direct cell lysis, and lymphocyte migration. In an attempt to determine the role of LFA-1 during RSV infection, we treated BALB/c mice with monoclonal antibodies to LFA-1 at days -1, +1, and +4 relative to primary RSV infection. Anti-LFA-1 treatment during primary RSV infection led to reduced illness and delayed clearance of virus-infected cells. CTLs from RSV-infected mice that were treated with anti-LFA-1 exhibited diminished cytolytic activity and reduced gamma interferon production. In addition, studies with BrdU (5-bromo-2'-deoxyuridine)- and CFSE [5-(and 6)-carboxyfluorescein diacetate succinimidyl ester]-labeled lymphocytes showed that anti-LFA-1 treatment led to delayed proliferation during RSV infection. These results indicate that LFA-1 plays a critical role in the initiation of the immune response to RSV infection by facilitating CTL activation. These results may prove useful in the development of new therapies to combat RSV infection or other inflammatory diseases.

* Corresponding author. Mailing address: Vaccine Research Center, NIAID, National Institutes of Health, Building 40, Room 2502, 40 Convent Dr., MSC 3017, Bethesda, MD 20892-3017. Phone: (301) 594-8468. Fax: (301) 480-2771. E-mail: bgraham{at}nih.gov.

{dagger} Present address: Cell Genesys, Foster City, CA 94404.

Journal of Virology, March 2004, p. 3014-3023, Vol. 78, No. 6
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.6.3014-3023.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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