ArticleEuropean journal of immunology2022
NLRP3 inflammasome triggers interleukin-37 release from human monocytes.
Article in European journal of immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- Interleukin-37 in Cancer Angiogenesis: Mechanisms, Therapeutic Potential, and Future Perspectives.Cancer reports (Hoboken, N.J.) · 2026Review
- The complex role of IL-37 in cancer pathogenesis: exploring its influence on hallmarks of cancer.Frontiers in immunology · 2026Review
- Updated insights into the molecular networks for NLRP3 inflammasome activation.Cellular & molecular immunology · 2025Review
- Pyroptosis: A spoiler of peaceful coexistence between cells in degenerative bone and joint diseases.Journal of advanced research · 2025Review
- Advances in understanding the role of interleukins in pulmonary fibrosis (Review).Experimental and therapeutic medicine · 2025Review
- Hyperuricemia-induced complications: dysfunctional macrophages serve as a potential bridge.Frontiers in immunology · 2025Review
- Potential pro-tumour cytokine in oral squamous cellular carcinoma: IL37.Journal of cellular and molecular medicine · 2024Article
- Research Progress on the Role and Mechanism of IL-37 in Liver Diseases.Seminars in liver disease · 2023Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
IL-37 is an anti-inflammatory member of the IL-1 family that dampens inflammation associated with many noncommunicable diseases. However, mechanisms of IL-37 regulation remain understudied. We aimed to investigate the enzymatic cleavage of IL-37 that potentiates extracellular signalling, as well as pathways of IL-37 secretion. In human monocytes, mature IL-37 (mIL-37) was released following canonical NLRP3 inflammasome activation. The release of IL-37 was blocked by inhibiting plasma membrane permeability and in gasdermin-D-deficient THP-1 cells. While the cleavage of IL-37 was found to be constitutive, the release of mIL-37 was blocked in NLRP3-deficient THP-1 cells and by NLRP3 inhibitor MCC950 in THP-1s and primary human monocytes. IL-37 secretion also occurred after 18-h exposure to LPS, independently of the alternative NLRP3 inflammasome. This LPS-dependent IL-37 secretion required plasma membrane permeability, but not conventional protein secretion apparatus. Mutagenesis of the suggested caspase-1 cleavage site (D20) or the proposed alternative cleavage site (V46) did not completely block IL-37 processing. Therefore, we propose a novel pathway in which IL-37 is cleaved by caspase-1-independent mechanisms and released following canonical and alternative NLRP3 inflammasome triggers by differential pathways.
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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.