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Institute of Medical Microbiology and Immunology, University of Copenhagen, Copenhagen, Denmark
CD40 ligand (CD40L) is an important molecule that is known to be
involved in T-B collaboration and certain aspects of cell-mediated
immunity. However, its role in antiviral immunity has not been clearly
defined as of yet. Therefore, mice with a targeted defect in the gene
encoding this molecule were infected with one of two strains of
lymphocytic choriomeningitis virus differing markedly in their capacity
to spread in the host. Infection with lymphocytic choriomeningitis
virus is initially controlled primarily by CD8+ effector
cells, whereas long-term immune surveillance also depends upon
CD4+ cells and B cells. Our results reveal that the primary
activation, clonal expansion, and differentiation of CD8+ T
cells does not require expression of CD40L. However, lack of expression
results in rapid impairment of CTL responsiveness and failure to
permanently control virus replication. This happens not only in mice
infected with the rapidly spreading virus strain but also at a late
stage in mice infected with the strain of more limited potential for
spreading. In the latter mice, virus replication is initially
controlled very efficiently, but high levels of virus can be detected
in the blood and internal organs 
6 mo after virus
inoculation. Since the impairment of immune function seems to be
more pronounced in CD40L-deficient mice than in mice lacking either
CD4+ cells or B cells, these results indicate that CD40L is
pivotal to sustain efficient antiviral immune surveillance, including
CD8+ T cells, and suggest that CD40L is critically involved
in cellular interactions in addition to T-B
cooperation.
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