Decreased IL-10 expression in stefin B-deficient macrophages is regulated by the MAP kinase and STAT-3 signaling pathways |
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| Authors: | Katarina Maher,Janja Zavr&scaron nik,Barbara Jerič-Kokelj,Olga Vasiljeva,Boris Turk,Nata&scaron a Kopitar-Jerala |
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| Affiliation: | 1. Department of Biochemistry, Molecular and Structural Biology, Jo?ef Stefan Institute, Ljubljana SI-1000, Slovenia;2. Jo?ef Stefan International Postgraduate School, Jamova 39, SI-1000 Ljubljana, Slovenia;3. Centre of Excellence for Integrated Approaches in Chemistry and Biology of Proteins (CIPKeBiP), Jamova 39, SI-1000 Ljubljana, Slovenia;4. Department of Chemistry and Biochemistry, Faculty of Chemistry and Chemical Technology, University of Ljubljana, Cesta v Mestni log 88A, SI-1000 Ljubljana, Slovenia |
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| Abstract: | Innate immune responses are tightly regulated to avoid excessive activation and subsequent inflammatory damage to the host, and interleukin-10 (IL-10) plays a crucial role in preventing inflammation. Stefin B (cystatin B) is an endogenous inhibitor of cysteine proteinases. In stefin B-deficient bone marrow-derived macrophages (BMDMs), we detected an increase in the induction of the LPS-induced pro-inflammatory signal nitric oxide (NO) but decreased IL-10 expression. The phosphorylation of ERK and p38 MAP-kinases was significantly decreased in stefin B-deficient macrophages, as was STAT-3 phosphorylation. These findings show that stefin B influences the expression of anti-inflammatory IL-10 in response to the TLR4 agonist LPS. |
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| Keywords: | Cystatin Interleukin-10 Lipopolysaccharide Macrophage MAP-kinase Nitric oxide |
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