| Literature DB >> 11754813 |
R J Riese1, G P Shi, J Villadangos, D Stetson, C Driessen, A M Lennon-Dumenil, C L Chu, Y Naumov, S M Behar, H Ploegh, R Locksley, H A Chapman.
Abstract
NK1.1(+) T cells develop and function through interactions with cell surface CD1 complexes. In I-A(b) mice lacking the invariant chain (Ii) processing enzyme, cathepsin S, NK1.1(+) T cell selection and function are impaired. In vitro, thymic dendritic cells (DCs) from cathepsin S(-/-) mice exhibit defective presentation of the CD1-restricted antigen, alpha-galactosylceramide (alpha-GalCer). CD1 dysfunction is secondary to defective trafficking of CD1, which colocalizes with Ii fragments and accumulates within endocytic compartments of cathepsin S(-/-) DCs. I-A(k), cathepsin S(-/-) mice do not accumulate class II-associated Ii fragments and accordingly do not display CD1 abnormalities. Thus, function of CD1 is critically linked to processing of Ii, revealing MHC class II haplotype and cathepsin S activity as regulators of NK T cells.Entities:
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Year: 2001 PMID: 11754813 DOI: 10.1016/s1074-7613(01)00247-3
Source DB: PubMed Journal: Immunity ISSN: 1074-7613 Impact factor: 31.745