Nonspecific Recruitment of Memory CD8 super(+) T Cells to the Lung Airways During Respiratory Virus Infections

• Published in: The Journal of immunology (1950) Vol. 170; no. 3; pp. 1423 - 1429
• Main Authors: Ely, KH, Cauley, L S, Roberts, AD, Brennan, J W, Cookenham, T, Woodland, D L
• Format: Journal Article
• Language: English
• Published: 01.02.2003
• ISSN: 0022-1767

Previous studies have shown that heterologous viral infections have a significant impact on pre-existing memory T cell populations in secondary lymphoid organs through a combination of cross-reactive and bystander effects. However, the impact of heterologous viral infections on effector/memory T cells in peripheral sites is not well understood. In this study, we have analyzed the impact of a heterologous influenza virus infection on Sendai virus-specific CD8 super(+) effector/memory cells present in the lung airways. The data show a transient increase in the numbers of Sendai virus nucleoprotein 324 332/K super(b)-specific CD8 super(+) memory T cells in the airways of the influenza-infected mice peaking around day 4 postinfection. Intratracheal transfer studies and 5-bromo-2'-deoxyuridine incorporation demonstrate that this increase is due to the recruitment of resting memory cells into the airways. In addition, the data show that these immigrating memory cells are phenotypically distinct from the resident memory T cells of the lung airways. A similar influx of nonproliferating Sendai virus nucleoprotein 324 332/K super(b)-specific CD8 super(+) memory T cells is also induced by a secondary (homologous) infection with Sendai virus. Together, these data suggest that inflammation can accelerate memory T cell migration to nonlymphoid tissues and is a part of the normal recall response during respiratory infections.