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/CCL3 in Regulation of T Cell-Mediated Immunity to Cryptococcus neoformans Infection1
*
Veterans Affairs Hospital and
Division of Pulmonary and Critical Care Medicine, The University of Michigan Medical School, Ann Arbor, MI 48109; and
Schering Plough Research Institute, Kenilworth, NJ 07033
Macrophage inflammatory protein-1
(MIP-1/CCL3) is a CC
chemokine required for optimal recruitment of leukocytes in response to
cryptococcal Ags. MIP-1 is expressed in the lungs by day 6 post
Cryptococcus neoformans infection and could play a role
in the development of cell-mediated immunity. To address this
possibility, wild-type (MIP-1+/+) mice and MIP-1
knockout (MIP-1-/-) mice were infected intratracheally
with a highly virulent strain of C. neoformans (145A).
MIP-1 message was detected in the lungs on days 3, 7, and 14 in
MIP-1+/+ mice, but it was undetectable in
MIP-1-/- mice. On day 16, MIP-1-/-
mice had a 7-fold increase in C. neoformans burden in
the lungs, but no decrease in pulmonary leukocyte recruitment.
MIP-1+/+ and MIP-1-/- mice had similar
numbers of recruited lymphocytes and monocytes/macrophages. Notably,
MIP-1-/- mice had a significantly greater number of
eosinophils. MIP-1-/- mice had extremely high levels
of serum IgE. This switch of immune response to a T2
phenotype was associated with enhanced IL-4 and IL-13 expression in the
lungs of MIP-1-/- mice compared with MIP-1
+/+ mice. Progression of pulmonary cryptococcosis in the
presence of nonprotective T2 immunity resulted in profound
lung damage in MIP-1-/- mice (eosinophilic crystal
deposition, destruction of lung parenchyma, and pulmonary hemorrhage).
Twelve-week survival was dramatically decreased in
MIP-1-/- mice. These studies, together with our
previous studies, demonstrate that MIP-1 plays a role in both the
afferent (T1/T2 development) and efferent
(T1-mediated leukocyte recruitment) phases of cell-mediated
immunity to C. neoformans.
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