ArticleImmunology2009
Identification of the most active interleukin-32 isoform.
Article in Immunology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 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.
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Who cites it
97 citing papers in PubMed, 180 citations in OpenAlex.
- Upregulation of IL-32γ in endothelial cells promotes macrophage recruitment and inflammatory progression in atherosclerosis.Scientific reports · 2026Article
- Spatial transcriptomics identifies IL-32 as a lipid droplet-associated cytokine linked to tubular injury in human diabetic kidney disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Role of IL-32 in RA pathology and potential as a drug target.Frontiers in immunology · 2026Review
- Quinic and Ferulic Acid-Loaded Chitosan Nanoparticles Attenuate Experimental Ulcerative Colitis by Modulating the IL-32/IL-33/IL-34 Axis and NF-κB Signaling.International journal of inflammation · 2026Article
- IL-32-producing CD8+ memory T cells define immunoregulatory niches in human cutaneous leishmaniasis.The Journal of clinical investigation · 2025Article
- Analysis of effector/memory regulatory T cells from arrhythmogenic cardiomyopathy patients identified IL-32 as a novel player in ACM pathogenesis.Cell death & disease · 2025Article
- A1AT dysregulation of metabolically stressed hepatocytes by Kupffer cells drives MASH and fibrosis.Experimental & molecular medicine · 2025Article
- Mini review: Interleukin-32 as a key mediator of type 1 diabetes pathogenesis.Frontiers in immunology · 2025Review
- Exploring the Involvement of New Members of the Interleukin Family in Cardiovascular Disease.Current cardiology reviews · 2025Review
- IL-32γ Induced Autophagy Through Suppression of MET and mTOR Pathways in Liver Tumor Growth Inhibition.International journal of molecular sciences · 2024Article
- mTOR activation induces endolysosomal remodeling and nonclassical secretion of IL-32 via exosomes in inflammatory reactive astrocytes.Journal of neuroinflammation · 2024Article
- Get Spliced: Uniting Alternative Splicing and Arthritis.International journal of molecular sciences · 2024Review
- IL-32 Drives the Differentiation of Cardiotropic CD4+ T Cells Carrying HIV DNA in People With HIV.The Journal of infectious diseases · 2024Article
- The Role of mRNA Alternative Splicing in Macrophages Infected withMolecules (Basel, Switzerland) · 2024Review
- Association of HBsAg levels with differential gene expression in NK, CD8 T, and memory B cells in treated patients with chronic HBV.JHEP reports : innovation in hepatology · 2024Article
- The regulation and potential role of interleukin-32 in tuberculous pleural effusion.Frontiers in immunology · 2024Article
- The Role of Pro-Inflammatory Mediator Interleukin-32 in Osteoclast Differentiation.Turkish journal of pharmaceutical sciences · 2023Article
- Circulating Interlukin-32 and Altered Blood Pressure Control in Individuals with Metabolic Dysfunction.International journal of molecular sciences · 2023Article
- Article
- IL-32 as a potential biomarker and therapeutic target in skin inflammation.Frontiers in immunology · 2023Review
37 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
Abstract
Cytokines are crucial in host defence against pathogens such as bacteria, viruses, fungi and parasites. A newly described cytokine, interleukin-32 (IL-32), induces various proinflammatory cytokines (tumour necrosis factor-alpha, IL-1beta, IL-6) and chemokines in both human and mouse cells through the nuclear factor-kappaB and p38 mitogen-activated protein kinase inflammatory signal pathway. The IL-32 primarily acts on monocytic cells rather than T cells. In an attempt to isolate the IL-32 soluble receptor, we used an IL-32 ligand-affinity column to purify neutrophil proteinase 3, which is a serine proteinase involved in many inflammatory diseases. IL-32 has biological activity associated with Mycobacterium tuberculosis and chronic proinflammatory diseases such as rheumatoid arthritis. IL-32 is transcribed as six alternative splice variants and the biological activity of each individual isoform remains unknown. Here, we cloned the complementary DNA of the four IL-32 isoforms (alpha, beta, gamma and delta) that are the most representative IL-32 transcripts. To produce recombinant protein with a high yield, the amino acids of two cysteine residues were mutated to serine residues, because serine residues are not conserved among different species. The multi-step purified recombinant IL-32 isoform proteins were assessed for their biological activities with different cytokine assays. The gamma isoform of IL-32 was the most active, although all isoforms were biologically active. The present study will provide a specific target to neutralize endogenous IL-32, which may contribute to basic and clinical immunology.
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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.