Abstract

The JHM strain of mouse hepatitis virus (JHMV) is rapidly cleared from the central nervous system (CNS) by CD8(+) T cells. In the absence of CD4(+) T cells, fewer CD8(+) T cells are found within the CNS in association with a coordinate increase in apoptotic lymphocytes. Previous data suggested that CD4(+) T cells may support CD8(+) T cells through secretion of interleukin-2 (IL-2). To determine the in vivo role of IL-2 during CNS infection, IL-2 signaling was inhibited via administration of a neutralizing IL-2-specific monoclonal antibody (mAb). In contrast to depletion of CD4(+) T cells, inhibition of IL-2 signaling did not influence CD8(+) T cell infiltration, effector cell function or survival within the CNS. These data suggest that the cellular immune response to acute neurotropic JHMV infection requires a distinct CD4(+) T cell component, but is independent of a requirement for IL-2 for induction, activation, recruitment, and/or maintenance of CD8(+) T cells within the CNS during acute infection.

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