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Respiratory syncytial virus infection suppresses lung CD8+ T-cell effector activity and peripheral CD8+ T-cell memory in the respiratory tract

Abstract

Respiratory syncytial virus (RSV) is a major cause of morbidity from respiratory infection in infants, young children and the elderly. No effective vaccine against RSV is currently available and studies of the natural history of RSV infection suggest repeated infections with antigenically related virus strains are common throughout an individual's lifetime. We have studied the CD8+ T-cell response during experimental murine RSV infection and found that RSV inhibits the expression of effector activity by activated RSV-specific CD8+ T cells infiltrating the lung parenchyma and the development of pulmonary CD8+ T-cell memory by interfering with TCR-mediated signaling. These data suggest a possible mechanism to explain the limited duration of protective immunity in RSV infection.

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Figure 1: Visualization and quantification of M2-specific CD8+ T cells during RSV infection in BALB/c mice.
Figure 2: Effector activity, antigen-dependant TCR downregulation and IL-2 rescue of M2-specific lung and spleen CD8+ T cells.
Figure 3: Perforin expression of M2-specific cells derived from the lung and in vitro stimulated splenocytes culture.

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Acknowledgements

We wish to acknowledge the expert and dedicated support of S. Gill in the completion of this work. The work was supported by USPHS grants to T.J.B.

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Correspondence to Thomas J. Braciale.

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Chang, J., Braciale, T. Respiratory syncytial virus infection suppresses lung CD8+ T-cell effector activity and peripheral CD8+ T-cell memory in the respiratory tract. Nat Med 8, 54–60 (2002). https://doi.org/10.1038/nm0102-54

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