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The Journal of Immunology, 2000, 165: 6429-6436.
Copyright © 2000 by The American Association of Immunologists

The Role of Macrophage Inflammatory Protein-1{alpha}/CCL3 in Regulation of T Cell-Mediated Immunity to Cryptococcus neoformans Infection1

Michal A. Olszewski*,{dagger}, Gary B. Huffnagle2,{dagger}, Roderick A. McDonald{dagger}, Dennis M. Lindell{dagger}, Bethany B. Moore{dagger}, Donald N. Cook{ddagger} and Galen B. Toews*,{dagger}

* Veterans Affairs Hospital and {dagger} Division of Pulmonary and Critical Care Medicine, The University of Michigan Medical School, Ann Arbor, MI 48109; and {ddagger} Schering Plough Research Institute, Kenilworth, NJ 07033

Macrophage inflammatory protein-1{alpha} (MIP-1{alpha}/CCL3) is a CC chemokine required for optimal recruitment of leukocytes in response to cryptococcal Ags. MIP-1{alpha} 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{alpha}+/+) mice and MIP-1{alpha} knockout (MIP-1{alpha}-/-) mice were infected intratracheally with a highly virulent strain of C. neoformans (145A). MIP-1{alpha} message was detected in the lungs on days 3, 7, and 14 in MIP-1{alpha}+/+ mice, but it was undetectable in MIP-1{alpha}-/- mice. On day 16, MIP-1{alpha}-/- mice had a 7-fold increase in C. neoformans burden in the lungs, but no decrease in pulmonary leukocyte recruitment. MIP-1{alpha}+/+ and MIP-1{alpha}-/- mice had similar numbers of recruited lymphocytes and monocytes/macrophages. Notably, MIP-1{alpha}-/- mice had a significantly greater number of eosinophils. MIP-1{alpha}-/- 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{alpha}-/- mice compared with MIP-1{alpha} +/+ mice. Progression of pulmonary cryptococcosis in the presence of nonprotective T2 immunity resulted in profound lung damage in MIP-1{alpha}-/- mice (eosinophilic crystal deposition, destruction of lung parenchyma, and pulmonary hemorrhage). Twelve-week survival was dramatically decreased in MIP-1{alpha}-/- mice. These studies, together with our previous studies, demonstrate that MIP-1{alpha} 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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