ArticleThe Journal of biological chemistry2009
Increased cytokine production in interleukin-18 receptor alpha-deficient cells is associated with dysregulation of suppressors of cytokine signaling.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 43 citations in OpenAlex.
- An antibody to IL-1 receptor 7 protects mice from LPS-induced tissue and systemic inflammation.Frontiers in immunology · 2024Article
- Methylation changes induced by a glycodendropeptide immunotherapy and associated to tolerance in mice.Frontiers in immunology · 2022Article
- IL-37b alleviates endothelial cell apoptosis and inflammation in Kawasaki disease through IL-1R8 pathway.Cell death & disease · 2021Article
- Negative Regulation of RNF90 on RNA Virus-Triggered Antiviral Immune Responses Targeting MAVS.Frontiers in immunology · 2021Article
- Article
- The Role, Involvement and Function(s) of Interleukin-35 and Interleukin-37 in Disease Pathogenesis.International journal of molecular sciences · 2018Review
- Oxymatrine Sensitizes the HaCaT Cells to the IFN-γ Pathway and Downregulates MDC, ICAM-1, and SOCS1 by Activating p38, JNK, and Akt.Inflammation · 2018Article
- Interleukin-18: Biological properties and role in disease pathogenesis.Immunological reviews · 2018Review
- Synthetic PreImplantation Factor (PIF) prevents fetal loss by modulating LPS induced inflammatory response.PloS one · 2017Article
- Suppression of innate inflammation and immunity by interleukin-37.European journal of immunology · 2016Review
- IL-37 requires the receptors IL-18Rα and IL-1R8 (SIGIRR) to carry out its multifaceted anti-inflammatory program upon innate signal transduction.Nature immunology · 2015Article
- Extracellular forms of IL-37 inhibit innate inflammation in vitro and in vivo but require the IL-1 family decoy receptor IL-1R8.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Sustained interleukin-1β exposure modulates multiple steps in glucocorticoid receptor signaling, promoting split-resistance to the transactivation of prominent anti-inflammatory genes by glucocorticoids.Mediators of inflammation · 2015Article
- The pathological role of IL-18Rα in renal ischemia/reperfusion injury.Laboratory investigation; a journal of technical methods and pathology · 2015Article
- Interleukin-18 mediates interleukin-1-induced cardiac dysfunction.American journal of physiology. Heart and circulatory physiology · 2014Article
- Article
- The interleukin-1 family: back to the future.Immunity · 2013Review
- IL-18 in inflammatory and autoimmune disease.Cellular and molecular life sciences : CMLS · 2013Review
- Interleukin-18 activates skeletal muscle AMPK and reduces weight gain and insulin resistance in mice.Diabetes · 2013Article
- Role of IL-18 in second-hand smoke-induced emphysema.American journal of respiratory cell and molecular biology · 2013Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Since interleukin (IL)-18 is a proinflammatory cytokine, mice lacking IL-18 or its ligand-binding receptor (IL-18R) should exhibit decreased cytokine and chemokine production. Indeed, production of IL-1alpha, IL-6, and MIP-1alpha was reduced in IL-18 knock-out (ko) mouse embryonic fibroblast (MEF)-like cells. Unexpectedly, we observed a paradoxical 10-fold increase in IL-1beta-induced IL-6 production in MEF cells from mice deficient in the IL-18R alpha-chain (IL-18Ralpha) compared with wild type MEF. Similar increases were observed for IL-1alpha, MIP-1alpha, and prostaglandin E2. Likewise, coincubation with a specific IL-18Ralpha-blocking antibody augmented IL-1beta-induced cytokines in wild type and IL-18 ko MEF. Stable lines of IL-18Ralpha-depleted human A549 cells were generated using shRNA, resulting in an increase of IL-1beta-induced IL-1alpha, IL-6, and IL-8 compared to scrambled small hairpin RNA. In addition, we silenced IL-18Ralpha with small interfering RNA in primary human blood cells and observed up to 4-fold increases in the secretion of lipopolysaccharide- and IL-12/IL-18-induced IL-1beta, IL-6, interferon-gamma, and CD40L. Mechanistically, despite increases in Stat1 and IL-6, induction of SOCS1 and -3 (suppressor of cytokine signaling 1 and 3) was markedly reduced in the absence of IL-18Ralpha. Consistent with these observations, activation of the p38alpha/beta and ERK1/2 MAPKs and of protein kinase B/Akt increased in IL-18Ralpha ko MEF, whereas the negative feedback kinase MSK2 was more active in IL-18 ko cells. These data reveal a role for SOCS1 and -3 in the seemingly paradoxical hyperresponsive state in cells deficient in IL-18Ralpha, supporting the concept that IL-18Ralpha participates in both pro- and anti-inflammatory responses and that an endogenous ligand engages IL-18Ralpha to deliver an inhibitory signal.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.