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-Deficient Mice1
* Department of Molecular Genetics, Biochemistry, and Microbiology,
Howard Hughes Medical Institute, and
Division of Infectious Diseases, Department of Internal Medicine, University of Cincinnati, Cincinnati, OH 45267;
Department of Microbiology and Immunology, Pennsylvania State University, Milton S. Hershey College of Medicine, Hershey, PA 17033; and
¶ Viral Immunology Section, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD 20892
Protein complexes of the 28-kDa proteasome activator (PA28) family activate the proteasome and may alter proteasome cleavage specificity. Initial investigations have demonstrated a role for the IFN-
-inducible PA28
/
complex in Ag processing. Although the noninducible and predominantly nuclear PA28 complex has been implicated in affecting proteasome-dependent signaling pathways, such as control of the mitotic cell cycle, there is no previous evidence demonstrating a role for this structure in Ag processing. We therefore generated PA28-deficient mice and investigated their immune function. PA28-/- mice display a slight reduction in CD8+ T cell numbers and do not effectively clear a pulmonary fungal infection. However, T cell responses in two viral infection models appear normal in both magnitude and the hierarchy of antigenic epitopes recognized. We conclude that PA28-/- mice, like PA28-/-/-/- mice, are deficient in the processing of only specific Ags.
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