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Published on: September 2, 2014
Decreased IL-10 expression in stefin B-deficient macrophages is regulated by the MAP kinase and STAT-3 signaling
Katarina Maher1, Janja Završnik1, Barbara Jerič-Kokelj1
1Department of Biochemistry, Molecular and Structural Biology, Jožef Stefan Institute, Ljubljana SI-1000, Slovenia; Jožef Stefan International Postgraduate School, Jamova 39, SI-1000 Ljubljana, Slovenia.
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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