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Interleukin-1 beta (IL-1β) also known as leukocytic pyrogen, leukocytic endogenous mediator, mononuclear cell factor, lymphocyte activating factor and other names, is a cytokine protein that in humans is encoded by the IL1B gene.
The nomenclature also proposes that IL-1F5 should be renamed to IL-36Ra, because it works as an antagonist to IL-36α, IL-36β and IL-36γ similar to how IL-1Ra works for IL-1α and IL-1β. Another revision was the renaming of IL-1F7 to IL-37 because this suppressing cytokine has many splicing variants , they should be called IL-37a, IL-37b and ...
The protein encoded by this gene is a decoy receptor for certain cytokines that belongs to the interleukin-1 receptor family. This protein binds interleukin-1α (IL1A), interleukin-1β (IL1B), and interleukin 1 receptor antagonist (IL1Ra), preventing them from binding to their regular receptors and thereby inhibiting the transduction of their signaling.
Ig-like domain is the part of receptor which is located extracellularly. There are minimal homologies in amino acid sequences of Ig-like domains between proteins of IL-1R family but they all show characteristic Ig-fold and two β-sheets joined together by disulfide bonds which form between cysteine residues.
Interleukin 10 (IL-10) is a protein that inhibits the synthesis of a number of cytokines, including IFN-gamma, IL-2, IL-3, TNF, and GM-CSF produced by activated macrophages and by helper T cells. In structure, IL-10 is a protein of about 160 amino acids that contains four conserved cysteines involved in disulphide bonds. [33]
Interleukin-1 receptor (IL-1R) is a cytokine receptor which binds interleukin 1. [1] Two forms of the receptor exist. The type I receptor is primarily responsible for transmitting the inflammatory effects of interleukin-1 (IL-1) while type II receptors may act as a suppressor of IL-1 activity by competing for IL-1 binding. [1]
Pro-inflammatory cytokines such as IL-1β, IL-6, and TNF-α also trigger pathological pain. [1] While IL-1β is released by monocytes and macrophages, it is also present in nociceptive DRG neurons. IL-6 plays a role in neuronal reaction to an injury. TNF-α is a well known proinflammatory cytokine present in neurons and the glia.
However, IL-23, IL-1B and retinoic acid present in the intestine can drive the differentiation of ILC1s back to ILC3s. [39] Evidence also suggests the ability of ILC2s to acquire the pro-inflammatory phenotype, with ILC2s producing IFN-γ present in the intestine of patients with Crohn’s disease, in response to certain environmental factors ...