Background IL-1b (Interleukin-1 beta, IL-1beta) is a potent inflammatory cytokine which has been well studied. Produced as a precursor, especially in myeloid cells and monocytes/macrophages, IL-1b is processed by cleavage with caspase-1, or ICE, from the 31 kD inactive precursor to the 18kD active mature form secreted from cells as an end-result of the inflammasome complex and activation sequence (1, 2). In response to various TLR ligands, myeloid cells or macrophages activate NLRP3 inflammasomes and secrete IL-1b. The rate of IL-1b processing has been correlated to redox state or levels of ROS generated (3, 4). IL-1b is directly involved in a variety of diseases -–auto-inflammatory diseases, acute inflammatory attacks such as ischemic injury in myocardial infarcts or in chronic inflammatory processes of atherosclerosis or Type 2 diabetes (5, 6). The ability to detect and quantitate active IL-1b is critical for understanding how to regulate its activity as a therapeutic target. |
Reference
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