Interleukin1beta

Interleukins (from Latin/Greek inter = between; leukos = white; kinein = to move) are a group of endogenous, short-chain regulatory proteins (cytokines) of the immune system (interleukin-1 to interleukin-35). Interleukins are mediators for the induction, progression and control of T-cell-mediated cytotoxic immune reactions and B-cell activation (antibody production).

Interleukin-1beta (in contrast to interleukin-1alpha) is only synthesized as a precursor protein after stimulation. Its expression is induced by the transcription factor NF-κB after exposure to innate immune cells, e.g. alarmins (=DAMPs). The synthesis of the interleukin-1beta precursor (and the interleukin-18 precursor) is triggered by the stimulation of cells of the innate immune system by Toll-like receptors (TLRs) or RIG-like receptors (RLRs). In a further step, the interleukin-1-beta precursor must be cleaved by a cysteine protease (caspase-1). Caspase-1 itself is released by special protein formations known as inflammasomes.

The activation of inflammasomes is triggered by cytosolic pattern recognition receptors (PRRs) that either originate from microbes (pathogen-associated molecular patterns/PAMPs) or are generated by the host cell itself (damage-associated molecular patterns/DAMPs/Broz P et al. 2016).

The secretion of interleukin-1beta therefore requires these two steps and the activation of various receptors in order to be activated. Under special circumstances, interleukin-1beta can also be processed by other proteases, e.g. in the case of severe neutrophilic inflammation.

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