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The Wistar Institute, Philadelphia, PA 19104
The notion that MHC class I- restricted CD8+ T (Tc)
cells are capable of resolving autonomously infections with influenza
virus is based largely on studies testing virus strains of low
pathogenicity in CD4+ T (Th) cell-deficient/depleted mice.
To test whether this holds also for pathogenic strains and to exclude
possible contributions by B cells, we analyzed PR8 infection in Th
cell-depleted B cell-deficient (µMT) mice. These mice, termed µMT
(-CD4), showed 80% mortality after infection with a small dose of
PR8, which resulted in insignificant mortality in intact or Th
cell-depleted BALB/c mice. Infection of µMT(-CD4) mice with a virus
of low pathogenicity was resolved without mortality, but, compared with
intact BALB/c mice, with delay of 
5 and 20 days from lung and
nose, respectively. The low mortality of Th cell-depleted BALB/c mice
suggested that B cells contributed to recovery in a Th-independent
manner. This was verified by showing that transfer of 8–10 million T
cell-depleted naive spleen cells into µMT(-CD4) mice 1 day before
infection reduced mortality to 0%. The mechanism by which B cells
improved recovery was investigated. We found no evidence that they
operated by improving the lung-associated Tc response. Treatment of
infected µMT(-CD4) mice with normal mouse serum spiked with
hemagglutinin-specific IgM did not reduce mortality. Taken together,
the data show that 1) the Tc response is capable of resolving
autonomously (in conjunction with innate defenses) influenza virus
infections, although with substantial delay compared with intact mice,
and 2) B cells can contribute to recovery by a Th-independent
mechanism.
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