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Deficient CD4⁺ T Cell Priming and Regression of CD8⁺ T Cell Functionality in Virus-Infected Mice Lacking a Normal B Cell Compartment ¹

Institute of Medical Microbiology and Immunology, University of Copenhagen, Copenhagen, Denmark

In this study, we investigate the state of T cell-mediated immunity in B cell-deficient (B^-/-) mice infected with two strains of lymphocytic choriomeningitis virus known to differ markedly in their capacity to persist. In B^-/- C57BL mice infected with the more persisting virus, virus-specific CD8⁺ T cells are initially generated that are qualitatively similar to those in wild-type mice. However, although cell numbers are well sustained over time, the capacity to produce cytokines is rapidly impaired. In similarly infected B^-/- BALB/c mice, virus-specific CD8⁺ T cells are completely deleted, indicating that host genotype influences the severity of the T cell defect. In B^-/- C57BL mice infected with the less persisting virus, CD8⁺ T cell dysfunction was not as pronounced, although it was clearly present. Most importantly, the appearance of dysfunctional CD8⁺ T cells clearly precedes recrudescence of detectable virus, indicating that the T cell defect is not simply a secondary event due to virus buildup resulting from the failure of B^-/- mice to produce neutralizing Abs. In contrast with CD8⁺ T cells, which initially respond almost as in wild-type mice, the priming of virus-specific CD4⁺ T cells was markedly impaired in B^-/- mice infected with either virus strain. Thus, our results indicate that B cells play an important role in antiviral immunity not only as Ab producers, but also in promoting an optimal and sustained T cell response. The T cell defects are likely to contribute to the chronic course of viral infection in B^-/- mice.

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