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Immunol Cell Biol. 2012 Oct;90(9):841-51. doi: 10.1038/icb.2012.29. Epub 2012 Jul 17.

Serpinb9 (Spi6)-deficient mice are impaired in dendritic cell-mediated antigen cross-presentation.

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1
Department of Biochemistry and Molecular Biology, Monash University, Clayton, Victoria, Australia.

Erratum in

  • Immunol Cell Biol. 2012 Oct;90(9):916.

Abstract

Serpinb9 (Sb9, also called Spi6) is an intracellular inhibitor of granzyme B (GrB) that protects activated cytotoxic lymphocytes from apoptosis. We show here that the CD8(+) subset of splenic dendritic cells (DC), specialized in major histocompatibility complex class I (MHC I) presentation of exogenous antigens (cross-presentation), produce high levels of Sb9. Mice deficient in Sb9 are unable to generate a cytotoxic T-cell response against cell-associated antigen by cross-presentation, but maintain normal MHC-II presentation to helper T cells. This impaired cross-priming ability is autonomous to DC and is evident in animals deficient in both Sb9 and GrB, indicating that this role of Sb9 in DC is GrB-independent. In Sb9-deficient mice, CD8(+) DC develop normally, survive as well as wild-type DC after antigenic challenge, and exhibit unimpaired capacity to take up antigen. Although the core processing machinery is unaffected, Sb9-deficient DC appear to process antigen faster. Our results point to a novel, GrB-independent role for Sb9 in DC cross-priming.

PMID:
22801574
DOI:
10.1038/icb.2012.29
[Indexed for MEDLINE]
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