Interleukin-1 beta (IL1 beta or IL1B) also known as catabolin, is a member of the interleukin 1 cytokine family. IL1 is a pleiotropic cytokine. It is involved in the inflammatory response, cell growth, and tissue repair in the cortex. The IL1 superfamily consists of three members, IL1A (IL1 alpha), IL1B (IL1 beta), and IL1 receptor antagonist (IL1Ra). In clinical, it has been reported that Interleukin (IL)-1 may influence Th1 / Th2 immune responsiveness and has been implicated in the establishment of a successful pregnancy. Proinflammatory interleukin (IL)-1 gene polymorphisms associated with high levels of IL-1beta activity increase the risk for hypochlorhydria and distal gastric carcinoma. IL1B polymorphisms may be involved in susceptibility to SSc. Moreover, the IL2-389-G allele may be a marker for the limited phenotype of systemic sclerosis (SSc).
Interleukin 1 receptor, type I (IL-1R1) also known as CD121a (Cluster of Differentiation 121a), is an interleukin receptor. IL-1R1/CD121a is a cytokine receptor that belongs to the interleukin 1 receptor family. This protein is a receptor for interleukin alpha (IL1A), interleukin beta (IL1B), and interleukin 1 receptor, type I (IL1R1/IL1RA). IL-1R1/CD121a is an important mediator involved in many cytokine induced immune and inflammatory responses. This protein has been characterized by pharmacological and molecular techniques in the mouse brain. The spindle-shaped astrocytes enclose the wound, separating the healthy from damaged neural tissue. The shape change and subsequent repair processes are IL-1β activity-dependent, acting through the IL-1 type 1 receptor (IL-1R1), as co-application of the IL-1type 1 receptor antagonist protein (IL-1ra) blocks IL-1β induced effects. In the spleen, a slight increase in IL-1R AcP and IL-1R1 was observed during the first hours following LPS stimulation. In conclusion, IL-1R AcP mRNA is expressed in the brain and in other tissues where IL-1R1/CD121a transcripts are found. However, the regulation of its expression is distinct from IL-1R1/CD121a. The high level of expression and the lack of regulation of IL-1R AcP transcripts in the brain under inflammatory conditions suggest that the protein might be constitutively expressed in excess.
The type I IL-1 receptor (IL-1 RI, designated IL-1 R1 and CD121a) is one of at least nine members of the IL-1 R family with anin the Toll/IL-1 R (TIR) superfamily. IL-1 RI is an 80 kDa type I transmembrane (TM) protein that binds the pleiotropic cytokines IL-1 alpha and IL-1 beta, plus the IL-1 receptor antagonist (IL-1 Ra). Signal transduction requires complex formation with an the IL-1 R accessory protein (IL-1 R AcP/IL-1 R3), another type I TM protein. This complex recruits the adaptor protein MyD88, to initiate signaling in the NF kappa B pathway. Rat IL-1 RI cDNA encodes a 576 amino acid (aa) protein that contains a 19 aa signal sequence, a 319 aa extracellular domain (ECD) with an three C2-type Ig-like domains, a 21 aa TM domain and a 217 aa cytoplasmic region with an a TIR domain. Rat IL-1 RI shares 83%, 65%, 60%, 60% and 54% aa identity with an Mouse, Human, canine, equine and bovine IL-1 RI, respectively. Two additional splice isoforms of rat IL-1 RI have been described. One has an N-terminus that is extended by 14 amino acids, but appears to have equivalent function. The other lacks the TM sequence and is secreted as an ~82 kDa protein that antagonizes the effect of IL-1 beta. Thus, the role of IL-1 in inflammation is under several levels of control, including expression and activation of IL-1 alpha and IL-1 beta, expression of IL-1 RI and its accessory and adaptor proteins, and inhibitory IL-1 R isoforms and decoys (1-6). IL-1 RI is expressed predominantly by T cells, fibroblasts, and endothelial cells and mediates acute phase inflammatory responses including fever.
Interleukin 1 receptor, type II (IL1R2) also known as CD121b (Cluster of Differentiation 121b) is a cytokine receptor that belongs to the interleukin-1 receptor family. This protein binds interleukin alpha (IL1A), interleukin beta (IL1B), and interleukin 1 receptor, type I (IL1R1/IL1RA), and acts as a decoy receptor that inhibits the activity of its ligands. The pleiotropic cytokine IL1 is produced to regulate development and maintenance of the inflammatory responses, and binds to specific plasma membrane receptors on cells. Two distinct types of IL1 receptors which are able to bind IL1 specifically have been identified, designated as IL1RI (IL1RA) and IL1RII (IL1RB). IL1R1 contributes to IL-1 signaling, whereas the IL-1R2/CD121b has no signaling property and acts as a decoy for IL-1. IL-1R2/CD121b structurally consisting of a ligand binding portion comprised of three Ig-like domains, a single transmembrane region, and a short cytoplasmic domain, is expressed in a variety of cell types including B lymphocytes, neutrophils, monocytes, large granular leukocytes and endothelial cells. Interleukin 4 (IL4) is reported to antagonize the activity of interleukin 1 by inducing the expression and release of this cytokine.
Interleukin 1 receptor, type I (IL-1R1) also known as CD121a (Cluster of Differentiation 121a), is an interleukin receptor. IL-1R1/CD121a is a cytokine receptor that belongs to the interleukin 1 receptor family. This protein is a receptor for interleukin alpha (IL-1α/IL-1F1), interleukin beta (IL1B), and interleukin 1 receptor, type I (IL1R1/IL1RA). IL-1R1/CD121a is an important mediator involved in many cytokines induced immune and inflammatory responses. This protein has been characterized by pharmacological and molecular techniques in the mouse brain. The spindle-shaped astrocytes enclose the wound, separating the healthy from damaged neural tissue. The shape change and subsequent repair processes are IL-1β activity-dependent, acting throμgh the IL-1 type 1 receptor (IL-1R1), as co-application of the IL-1type 1 receptor antagonist protein (IL-1ra) blocks IL-1β induced effects. In the spleen, a slight increase in IL-1R ACP and IL-1R1 was observed during the first hours following LPS stimulation. In conclusion, IL-1R AcP mRNA is expressed in the brain and in other tissues where IL-1R1/CD121a transcripts are found. However, the regulation of its expression is distinct from IL-1R1/CD121a. The high level of expression and the lack of regulation of IL-1R AcP transcripts in the brain under inflammatory conditions sμggest that the protein might be constitutively expressed in excess.
Lascia la tua email e seleziona le aree che vuoi seguire per ricevere novita di prodotto, approfondimenti tecnici e promozioni piu pertinenti.
Puoi scegliere le macro-aree Life Science e Diagnostica oppure le singole specializzazioni.
Seleziona uno o piu ambiti di interesse per ricevere comunicazioni piu utili e mirate.
Aggiornamenti su ricerca, strumentazione e applicazioni per il mondo Life Science.
Novita, approfondimenti e promozioni per laboratori diagnostici e flussi operativi.
2025 TEMA Ricerca - All Rights Reserved.
