Abstract

Activation of p38 MAP kinase in T cells leads to increased interferon-γ production in CD4 + and CD8 + T cells, and the selective cell death of CD8 + T cells. To address the role of p38 MAP kinase activation in T cells during an in vivo immune response, we examined the response against the influenza virus in transgenic mice expressing a constitutively activated MKK6 (MKK6(Glu)), an upstream activator of p38 MAP kinase. Activated CD4 + T cells accumulate in the lung and mediastinal lymph node of both wild-type and MKK6(Glu) transgenic mice upon intranasal inoculation with the influenza virus. MKK6(Glu) CD8 + T cells, however, disappear rapidly from the mediastinal lymph node but accumulate in the lung tissue. We demonstrate that interleukin-6, a cytokine produced by lung epithelial cells, partially protects CD8 + T cells from the cell death induced by p38 MAP kinase activation. During the influenza infection in MKK6(Glu) transgenic mice, reduced virus titers were also observed despite a normal B-cell antibody response. These results indicate that the activation of p38 MAP kinase in T cells affects the in vivo antiviral immune response.

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