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Immune Modulation In Sepsis
Published in Thomas F. Kresina, Immune Modulating Agents, 2020
Janet M. J. Hammond, Peter D. Potgieter
The two IL-1 receptors differ considerably in distribution, with the type I receptor being found on the majority of cells, including T cells, fibroblasts, and endothelial cells, where it is important in signal transduction after binding to IL-1. The type II receptor is found mainly on neutrophils, monocytes, B cells, and bone marrow progenitor cells. This receptor has no signal transduction function and is thought to act as a decoy receptor, to reduce the amount of active IL-1. The extracellular domain of the type II receptor is also shed by neutrophils and monocytes as a soluble receptor, and these receptors bind with circulating IL-lb, thereby inhibiting its activity [71].
Immediate Cytokine Responses to Endotoxin: Tumor Necrosis Factor-α and the lnterleukin-1 Family
Published in Helmut Brade, Steven M. Opal, Stefanie N. Vogel, David C. Morrison, Endotoxin in Health and Disease, 2020
The IL-1 family members are presently IL-1β, IL-1α, and IL-lRa. They are considered a family primarily because they bind to the same receptor (the IL-1 receptor type I, IL-1RI). They also bind to the IL-1R type II decoy receptor (albeit with quite different affinities compared to the IL-1RI). The IL-1 receptor signaling complex is comprised of the IL-1 ligand binding IL-1RI and the IL-1R accessory protein (IL-lR-AcP), similar to the IL-2 receptor complex in which the p55 ligand binding IL-2Rα forms a complex with the p75 IL-2Rβ. Although the three IL-1 cytokines share less than 30% primary amino acid sequence homologies, they are structurally very similar since each is an all-β-pleated, barrel-like form. In that regard, two other cytokines have all-β-pleated forms: acidic fibroblast growth factor and IL-18. Fibroblast growth factor is not part of the IL-1 family because this growth factor does not bind to IL-1 receptors. However, recent studies suggest that IL-18 may now have to be considered part of the IL-1 family. This is based on the finding that IL-18 is the natural ligand for the IL-1 receptor family member called IL-lR-related protein (IL-1Rrp) (57).
The Monocyte Chemoattractant Protein Family
Published in Richard Horuk, Chemoattractant Ligands and Their Receptors, 2020
Alberto Mantovani, Silvano Sozzani, Paul Proost, Jo Van Damme
Examination of macrophage function and inflammation in neoplastic disorders, as well as in other inflammatory conditions, reveals a paradoxical situation in which recruitment at the tumor site coexists with a systemic defect in the ability to mount local inflammatory reactions.6,119 We speculated that chemokines produced continuously in tumors may contribute also to the systemic impairment of macrophage function observed in advanced neoplasia.6 In support of this hypothesis, chemoat-tractants were recently found to cause rapid release of the IL-1 decoy receptor and of the p75 TNF receptor,120,121 which could buffer the action of these inflammatory mediators.
Development of ACE2 loaded decoy liposomes and their effect on SARS-CoV-2 for Covid-19 treatment
Published in Pharmaceutical Development and Technology, 2022
Sema Arisoy, Meryem Kocas, Tansel Comoglu, Ismail Guderer, Sreeparna Banerjee
Decoy receptors function as 'molecular sinks' that bind to viruses and reduce circulating titers during infection. Decoys can make individual low affinity interactions with a particular pathogen, but multimerization creates many more interactions by increasing the overall avidity of the virus-bait interaction. This principle has been demonstrated with sialic acid decoys for the influenza virus (Rao et al. 2020). Hendricks et al. (2013) showed that liposomes containing sialylneolacto-N-tetraose c (LSTc) had a higher avidity for influenza than single monovalent LSTc. Decoy liposomes could bind directly to Influenza A Virus (IAV) virions and these bound virions could not bind to epithelial cells bearing sialic acid, suggesting that decoy liposomes could specifically block IAV infection.
Approaches for refining and furthering the development of CAR-based T cell therapies for solid malignancies
Published in Expert Opinion on Drug Discovery, 2021
Immunosuppressive mechanisms within the TME can also be neutralized by expression of decoy receptors. Many tumors are known to secrete the immunosuppressive cytokine, TGF-β which can interfere with CAR T cell function. Blockade of TGF-β can be achieved by expression of a dominant negative TGF-β receptor-II (dnTGF-βRII) which acts as a ‘sink’ for TGF-β within the TME. Co-expression of dnTGF-βRII alongside a PSMA targeting CAR promoted T cell proliferation and enhanced anti-tumor responses in vivo [93]. The therapeutic potential of a dominant negative PD-1 decoy receptor has also been demonstrated. T cells that expressed dominate negative PD-1 and an anti-CD19 CAR showed superior cytotoxicity in vitro and induced remission in 3 diffuse large B cell lymphoma patients [94].
Anti-inflammatory activities of a new VEGF blocker, Conbercept
Published in Immunopharmacology and Immunotoxicology, 2021
Decoy receptor drugs are a class of drugs designed according to the interaction between extracellular soluble receptors and ligands and can efficiently block specific signaling pathways. The effect of these drugs depends on the binding affinity of the extracellular soluble receptor to its specific ligand. Conbercept is a novel decoy receptor protein that is composed of VEGF receptor 1 and VEGF receptor 2 extracellular domains with the Fc region of a human immunoglobulin. It shows a remarkable anti-angiogenic effect. We want to know whether Conbercept could show the effect on chronic inflammation and acute inflammation. The activity of Conbercept against chronic inflammation was assessed by collagen-induced arthritis in rats. The effect of Conbercept against acute inflammation was evaluated using a mice ear swelling test. Our data indicated that Conbercept inhibited both chronic inflammation and acute inflammation.