The DOI matches its Crossref record; 228 of the 228 references it cites were found in a registry or an index.
Interleukin‐18: Biological properties and role in disease pathogenesis
Open accessAbstract
Summary: Initially described as an interferon (IFN)γ‐inducing factor, interleukin (IL)‐18 is indeed involved in Th1 and NK cell activation, but also in Th2, IL‐17‐producing γδ T cells and macrophage activation. IL‐18, a member of the IL‐1 family, is similar to IL‐1β for being processed by caspase 1 to an 18 kDa‐biologically active mature form. IL‐18 binds to its specific receptor (IL‐18Rα, also known as IL‐1R7) forming a low affinity ligand chain. This is followed by recruitment of the IL‐18Rβ chain. IL‐18 then uses the same signaling pathway as IL‐1 to activate NF‐kB and induce inflammatory mediators such as adhesion molecules, chemokines and Fas ligand. IL‐18 also binds to the circulating high affinity IL‐18 binding protein (BP), such as only unbound free IL‐18 is active. IL‐18Rα may also bind IL‐37, another member of the IL‐1 family, but in association with the negative signaling chain termed IL‐1R8, which transduces an anti‐inflammatory signal. IL‐18 BP also binds IL‐37 and this acts as a sink for the anti‐inflammatory properties of IL‐37. There is now ample evidence for a role of IL‐18 in various infectious, metabolic or inflammatory diseases such as influenza virus infection, atheroma, myocardial infarction, chronic obstructive pulmonary disease, or Crohn's disease. However, IL‐18 plays a very specific role in the pathogenesis of hemophagocytic syndromes (HS) also termed Macrophage Activation Syndrome. In children affected by NLRC 4 gain‐of‐function mutations, IL‐18 circulates in the range of tens of nanograms/mL. HS is treated with the IL‐1 Receptor antagonist (anakinra) but also specifically with IL‐18 BP. Systemic juvenile idiopathic arthritis or adult‐onset Still's disease are also characterized by high serum IL‐18 concentrations and are treated by IL‐18BP.
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Signaling pathways and targeted therapy for myocardial infarction
Zhang, Q., Wang, L., Wang, S., Cheng, H., Xu, L., Pei, G., Wang, Y., Fu, C., Jiang, Y., He, C., et al. (2022) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-022-00925-z · Cited by 831
Genomic and drug target evaluation of 90 cardiovascular proteins in 30,931 individuals
Folkersen, L., Gustafsson, S., Wang, Q., Hansen, D. H., Hedman, Å. K., Schork, A., Page, K., Zhernakova, D. V., Wu, Y., Peters, J., et al. (2020) · Nature Metabolism · doi:10.1038/s42255-020-00287-2 · Cited by 705
The NLRP3 inflammasome in acute myocardial infarction
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The Immunology of Macrophage Activation Syndrome
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Metadata
- Authors
- Kaplanski, G.
- Venue
- Immunological Reviews
- Publisher
- Wiley
- Published
- 2017-12-16
- Volume
- 281
- Issue
- 1
- Pages
- 138-153
- ISSN
- 0105-2896 (ISSN-L)
- 1600-065X
- OpenAlex
- W2781447571
- Cited by
- 606
- References
- 228
- FWCI
- 3.89
- Type
- journal article
- Language
- en
- Open access
- bronze
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