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Cathepsin C limits acute viral infection independently of NK cell and CD8+ T-cell cytolytic function.

Abstract
Destruction of target cells by cytotoxic T lymphocytes (CTLs) or natural killer (NK) cells requires the coordinated action of the pore forming protein perforin (Pfp) and the granzyme (Gzm) family of serine proteases. The activation of a number of serine proteases, including GzmA and B, is predominately mediated by cathepsin C (CatC). Deficiencies in CatC-null mice were therefore expected to replicate the defects observed in GzmAB-deficient mice. We have previously determined that GzmAB-deficient mice exhibit increased susceptibility to murine cytomegalovirus (MCMV) infection. Here, we have compared the ability of CatC(-/-) mice to control MCMV infection with that of GzmAB-deficient animals. We found that CatC(-/-) mice have organ-specific defects in the ability to control MCMV replication, a phenotype that is distinct to that observed in GzmAB(-/-) mice. Significantly, the cytolytic function of CatC-deficient NK cells and CTLs elicited during infection was indistinguishable from that of wild-type cells. Hence, CatC is involved in limiting MCMV replication; however, this effect is independent of its role in promoting effector cytolytic activity. These data provide evidence for a novel and unexpected role of CatC during viral infection.
AuthorsChristopher E Andoniou, Peter Fleming, Vivien R Sutton, Joseph A Trapani, Mariapia A Degli-Esposti
JournalImmunology and cell biology (Immunol Cell Biol) Vol. 89 Issue 4 Pg. 540-8 (May 2011) ISSN: 1440-1711 [Electronic] United States
PMID20975734 (Publication Type: Journal Article)
Chemical References
  • Antigens
  • Cathepsin C
Topics
  • Animals
  • Antigens (immunology)
  • Cathepsin C (genetics, metabolism)
  • Cell Line
  • Cytomegalovirus Infections (immunology)
  • Cytotoxicity, Immunologic (genetics, immunology)
  • Gene Deletion
  • Killer Cells, Natural (immunology)
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Muromegalovirus (physiology)
  • Neutrophils (immunology)
  • T-Lymphocytes, Cytotoxic (immunology)
  • Virus Replication (genetics, immunology)

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