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Departments of
*
Pathology and
Internal Medicine, University of New Mexico School of Medicine, Albuquerque, NM 87131;
Division of Pulmonary Medicine, University of Michigan Medical School, Ann Arbor, MI; and
§
Torrey Pines Institute for Molecular Studies, San Diego, CA 92121
A murine pulmonary infection with Cryptococcus
neoformans (Cne) has been used to determine mechanisms
regulating effective T cell-mediated immunity in the lungs. In BALB/c
and C.B-17 mice, following intratracheal deposition of Cne, the fungus
initially grows rapidly and is then progressively cleared from the
lungs. Cne clearance in C.B-17 mice requires CD4 and CD8 T cells,
IFN-
, and NO. Clearance in congenic BALB/c mice proceeds more slowly
than in C.B-17 mice, even though the only genetic difference between
these strains is at the Ig H chain-containing region of chromosome 12.
Examination of the pulmonary immune response in the two strains
revealed that both cleared lung Cne by T cell-dependent mechanisms and
generated equivalent levels of NO. Furthermore, both strains recruited
equal numbers of macrophages, lymphocytes, and neutrophils to the
lungs, although BALB/c mice recruited higher numbers of eosinophils.
Notably, leukocytes isolated from BALB/c lungs during infection
secreted lower levels of IFN- and higher levels of the Th2 cytokines
IL-4 and IL-5 as compared with lung leukocytes from C.B-17 mice.
Furthermore, serum levels of IgM, IgG1, IgG2a, and IgG3 anti-Cne
Abs generated during infection were significantly greater in BALB/c
mice than C.B-17 mice. These data suggest that although both BALB/c and
C.B-17 mice clear pulmonary cryptococcosis through T cell-mediated
mechanisms, Ig H chain-linked genes in BALB/c mice are associated with
a decreased effectiveness of the host response, which we suggest might
influence the balance in Th1/Th2 T cell subset development or increase
anti-Cne Abs, or both.
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