Decreased IL-10 expression in stefin B-deficient macrophages is regulated by the MAP kinase and STAT-3 signaling pathways

作者：Maher Katarina; Zavrsnik Janja; Jeric Kokelj Barbara; Vasiljeva Olga; Turk Boris; Kopitar Jerala Natasa^*

来源：FEBS LETTERS, 2014, 588(5): 720-726.

DOI：10.1016/j.febslet.2014.01.015

• Cystatin
• Interleukin-10
• Lipopolysaccharide
• Macrophage
• MAP-kinase
• Nitric oxide

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.

• 出版日期2014-3-3