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An Altered T Cell Repertoire in MECL-1-Deficient Mice¹

Michael Basler^*, Jacqueline Moebius^*, Laura Elenich, Marcus Groettrup^2,* and John J. Monaco

^* Division of Immunology, Department of Biology, University of Constance, Konstanz, Germany; and Department of Molecular Genetics, University of Cincinnati College of Medicine, Cincinnati, OH 45267

Immunoproteasome subunits low-molecular mass polypeptide (LMP)2 and LMP7 affect Ag presentation by MHC class I molecules. In the present study, we investigated the function of the third immunosubunit LMP10/multicatalytic endopeptidase complex-like (MECL)-1 (2i) in MECL-1 gene-targeted mice. The number of CD8⁺ splenocytes in MECL-1^–/– mice was 20% lower than in wild-type mice. Infection with lymphocytic choriomeningitis virus (LCMV) elicited a markedly reduced cytotoxic T cell (CTL) response to the LCMV epitopes GP276–286/D^b and NP205–212/K^b in MECL-1^–/– mice. The weak CTL response to GP276–286/D^b was not due to an impaired generation of this epitope but was attributed to a decreased precursor frequency of GP276–286/D^b-specific T cells. The expansion of TCR-V10⁺ T cells, which contain GP276–286/D^b-specific cells, was reduced in LCMV-infected MECL-1^–/– mice. Taken together, our data reveal an in vivo function of MECL-1 in codetermining the T cell repertoire for an antiviral CTL response.

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