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Respiratory Medicine, National Heart and Lung Institute, Imperial College of Science, Technology and Medicine, London, United Kingdom
In BALB/c mice, sensitization with the attachment protein (G) of
respiratory syncytial virus (RSV) leads to CD4+ T
cell-mediated lung eosinophilia during subsequent challenge with RSV.
To determine the host genetic influences on this model of lung
eosinophilia, we tested 15 different inbred mouse strains. Eosinophilia
developed in all H-2d (BALB/c, DBA/2n, and B10.D2), but not
in H-2k (CBA/Ca, CBA/J, C3H, BALB.K, or B10.BR) mouse
strains. Among H-2b mice, 129 and BALB.B developed
eosinophilia, whereas C57BL/6 and C57BL/10 did not. Testing first
generation crosses between sensitive and resistant strains showed that
eosinophilia developed in all H-2dxk
(n = 5), irrespective of background genes, but not
in H-2dxb (n = 2) mice. In vivo
depletion of CD8+ T cells or IFN-
rendered C57BL/6, but
not BALB.K mice, susceptible to eosinophilia. Analysis of B10
recombinant mice showed that the Dd allele (in B10.A(5R)
mice) prevented CD8+ T cell accumulation in the lung,
resulting in intense lung eosinophilia. However, the Db
allele (in B10.A(2R) and B10.A(4R) mice) supported CD8+ T
cell expansion and prevented eosinophilia. Intracellular cytokine
staining showed that lung eosinophilia correlated with reduced IFN-
and increased IL-10 expression in lung T cells. These results are
compatible with the unifying model that Th2 cells mediate the disease
but can be inhibited by CD8+ T cells secreting IFN-. Our
findings have important implications for the development of protective,
nonpathogenic vaccines for RSV disease.
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