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Molecular and Cellular Biology, January 2005, p. 789-796, Vol. 25, No. 2
0270-7306/05/$08.00+0 doi:10.1128/MCB.25.2.789-796.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
Divisions of Gastroenterology,1 Rheumatology and Allergy, Department of Internal Medicine, University of California, Davis, California,2 Department of Pediatrics, Yale Child Health Research Center, Yale University School of Medicine, New Haven, Connecticut3
Received 28 July 2004/ Accepted 12 October 2004
PRSS16 is a serine protease expressed exclusively in cortical thymic epithelial cells (cTEC) of the thymus, suggesting that it plays a role in the processing of peptide antigens during the positive selection of T cells. Moreover, the human PRSS16 gene is encoded in a region near the class I major histocompatibility complex (MHC) that has been linked to type 1 diabetes mellitus susceptibility. The mouse orthologue Prss16 is conserved in genetic structure, sequence, and pattern of expression. To study the role of Prss16 in thymic development, we generated a deletion mutant of Prss16 and characterized T-lymphocyte populations and MHC class II expression on cortical thymic epithelial cells. Prss16-deficient mice develop normally, are fertile, and show normal thymic morphology, cellularity, and anatomy. The total numbers and frequencies of thymocytes and splenic T-cell populations did not differ from those of wild-type controls. Surface expression of MHC class II on cTEC was also similar in homozygous mutant and wild-type animals, and invariant chain degradation was not impaired by deletion of Prss16. These findings suggest that Prss16 is not required for quantitatively normal T-cell development.
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