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Sökning: WFRF:(Benedyk K.)

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1.
  • 2017
  • swepub:Mat__t
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2.
  • Maresz, K. J., et al. (författare)
  • Porphyromonas gingivalis Facilitates the Development and Progression of Destructive Arthritis through Its Unique Bacterial Peptidylarginine Deiminase (PAD)
  • 2013
  • Ingår i: Plos Pathogens. - : Public Library of Science (PLoS). - 1553-7374. ; 9:9
  • Tidskriftsartikel (refereegranskat)abstract
    • Rheumatoid arthritis and periodontitis are two prevalent chronic inflammatory diseases in humans and are associated with each other both clinically and epidemiologically. Recent findings suggest a causative link between periodontal infection and rheumatoid arthritis via bacteria-dependent induction of a pathogenic autoimmune response to citrullinated epitopes. Here we showed that infection with viable periodontal pathogen Porphyromonas gingivalis strain W83 exacerbated collagen-induced arthritis (CIA) in a mouse model, as manifested by earlier onset, accelerated progression and enhanced severity of the disease, including significantly increased bone and cartilage destruction. The ability of P. gingivalis to augment CIA was dependent on the expression of a unique P. gingivalis peptidylarginine deiminase (PPAD), which converts arginine residues in proteins to citrulline. Infection with wild type P. gingivalis was responsible for significantly increased levels of autoantibodies to collagen type II and citrullinated epitopes as a PPAD-null mutant did not elicit similar host response. High level of citrullinated proteins was also detected at the site of infection with wild-type P. gingivalis. Together, these results suggest bacterial PAD as the mechanistic link between P. gingivalis periodontal infection and rheumatoid arthritis.
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3.
  • Los, Marek Jan, et al. (författare)
  • Anticancer drugs of tomorrow : apoptotic pathways as targets for drug design
  • 2003
  • Ingår i: Drug Discovery Today. - : Elsevier. - 1359-6446 .- 1878-5832. ; 8:2, s. 67-77
  • Tidskriftsartikel (refereegranskat)abstract
    • Apoptosis or programmed cell death is a set of ordered events that enables the selective removal of cells from tissue and is essential for homeostasis and proper function of multicellular organisms. Components of this signaling network, which include ligands, such as CD95, tumor necrosis factor (TNF) and TNF-related apoptosis-inducing ligand, as well as downstream molecules, such as caspases, Bcl-2 family members, and inhibitor-of-apoptosis proteins, which trigger and regulate apoptosis, are crucial targets for conventional drug development and gene therapy of cancer and other diseases. Here, we focus on apoptotic pathways and propose new potential molecular targets that could prove effective in controlling cell death in the clinical setting.
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