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The innate immune system combats tissue injury and infection by activating the proinflammatory responses involving the humoral complement system, granulocytes, macrophages and vascular endothelial cells (VEC)(Newton and Dixit, 2012; Zhu et al., 2012). Macrophages mediate proinflammatory responses by releasing inflammatory cytokines such as IL-1β. Once secreted, IL-1β paracrinically acts on the VEC and massively change their functions. These perturbations include a change from the anticoagulant phenotype to a procoagulant state, enhanced expression of vasoactive substances, cell adhesion molecules as well as inflammatory mediators including chemoattractants, and endothelial barrier dysfunction causing microvascular leakage (Pober and Sessa, 2007). Although essential for the effective immune defense, uncontrolled or chronic inflammatory response causes tissue damage and loss of organ function (Lon et al., 2012). Increased IL-1β expression and an aberrantly activated IL-1β signaling explicitly correlates with disease progression in a broad spectrum of local or systemic acute and chronic inflammatory diseases such as severe systemic inflammatory response syndrome, sepsis, inflammatory bowel disease and rheumatoid arthritis, and malignancies such as myeloma. In such diseases, blocking IL-1β signaling with naturally occurring IL-1 receptor (IL-1R) antagonist (IL-1Ra) Anakinra or neutralization with anti-IL-1β monoclonal antibody leads to abrupt and sustained decrease in disease severity (Dinarello, 2011). The classical IL-1β pathway involves the binding of IL-1β to IL-1R that results in the recruitment of the adapter …