Human Interleukin 1 Beta (IL1B) Protein

Background

IL1B is a major pro-inflammatory cytokine that belongs to the IL-1 family and plays a central role in inflammation, fever induction, and host defense. It is synthesized as an inactive precursor (pro-IL1B) in response to pathogen-associated molecular patterns (PAMPs) or damage-associated molecular patterns (DAMPs) and is cleaved into its active form by caspase-1 through inflammasome activation. IL1B binds to its receptor IL1R1, forming a signaling complex with IL1RAP, which activates downstream NF-κB, MAPK, and JNK pathways to drive the expression of cytokines, chemokines, and acute-phase proteins. IL1B is predominantly produced by activated monocytes, macrophages, and dendritic cells during infections, tissue damage, or inflammatory conditions. It plays a critical role in immune cell recruitment, pathogen clearance, and tissue repair, but excessive IL1B signaling leads to chronic inflammation, autoimmune disorders, and tumor progression. Dysregulation of IL1B is implicated in diseases such as rheumatoid arthritis, gout, and neuroinflammation. Knockout studies demonstrate impaired inflammatory responses, reduced cytokine production, and weakened host defense, highlighting IL1B's essential role in immune activation, inflammation, and disease pathogenesis.