ReviewCurrent opinion in allergy and clinical immunology2013
Role of interleukin-32 in chronic rhinosinusitis.
Review in Current opinion in allergy and clinical immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed, 12 citations in OpenAlex.
- IL-32 exacerbates adenoid hypertrophy via activating NLRP3-mediated cell pyroptosis, which promotes inflammation.Molecular medicine reports · 2021Article
- Cytokine Patterns and Endotypes in Acute and Chronic Rhinosinusitis.Current allergy and asthma reports · 2016Review
- IL-32: A Novel Pluripotent Inflammatory Interleukin, towards Gastric Inflammation, Gastric Cancer, and Chronic Rhino Sinusitis.Mediators of inflammation · 2016Review
- Significant association between IL-32 gene polymorphisms and susceptibility to endometrial cancer in Chinese Han women.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- Preliminary characterization of IL32 in basal-like/triple negative compared to other types of breast cell lines and tissues.BMC research notes · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
purpose of reviewIL-32 is a recently described proinflammatory cytokine and has been reported to be involved in inflammatory diseases. The purpose of this review is to discuss the role of IL-32 in chronic rhinosinusitis (CRS). RECENT
findingsTwo groups have recently reported data regarding the expression of IL-32 in CRS. IL-32 was induced by IFN-γ, TNF-α, dsRNA, and incubation with Th1 cells in primary nasal epithelial cells. IL-32 may be elevated in epithelial cells from patients with CRS without nasal polyps. IL-32 was significantly elevated in whole sinonasal tissue samples of nasal polyps compared with control tissue. IL-32 mRNA expression positively correlated with mRNA for CD3 and macrophage mannose receptor in nasal polyp tissue. Immunohistochemical studies demonstrated localization of IL-32 in epithelium, CD3(+) and CD68(+) cells, suggesting that epithelial cells, T cells, and macrophages are the major IL-32-producing cells in CRS. Activation of these cell types may trigger IL-32-related inflammation in CRS. SUMMARY: Elevated levels of IL-32 may play a role in the pathogenesis of CRS through its role as a proinflammatory cytokine and as an endogenous enhancer of pathogen-dependent cytokine production.
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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.