ArticleBlood2011
Inhibition of IL-32 activation by α-1 antitrypsin suppresses alloreactivity and increases survival in an allogeneic murine marrow transplantation model.
Article in Blood, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 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
43 citing papers in PubMed, 76 citations in OpenAlex.
- Biomarker-guided preemption of steroid-refractory graft-versus-host disease with α-1-antitrypsin.Blood advances · 2020Trial
- IL-32 as a potential biomarker and therapeutic target in cardiovascular disease.Frontiers in immunology · 2026Review
- Role of IL-32 in RA pathology and potential as a drug target.Frontiers in immunology · 2026Review
- Alpha-1 Antitrypsin Mediates Spontaneous Resolution of Acute Gouty Inflammation Via Inhibiting Caspase 3/GSDME-dependent Macrophage Pyroptosis.Inflammation · 2025Article
- Graft-Versus-Host Disease Mouse Models: A Clinical-Translational Perspective.Methods in molecular biology (Clifton, N.J.) · 2025Review
- Analysis of alpha-1-antitrypsin (AAT)-regulated, glucocorticoid receptor-dependent genes in macrophages reveals a novel host defense function of AAT.Physiological reports · 2024Article
- Secondary Neoplasms After Hematopoietic Cell Transplant for Sickle Cell Disease.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2023Article
- IL-32 as a potential biomarker and therapeutic target in skin inflammation.Frontiers in immunology · 2023Review
- Mesenchymal stromal cells and alpha-1 antitrypsin have a strong synergy in modulating inflammation and its resolution.Theranostics · 2023Article
- Therapeutic Potential of Alpha-1 Antitrypsin in Type 1 and Type 2 Diabetes Mellitus.Medicina (Kaunas, Lithuania) · 2021Review
- Placenta-derived IL-32β activates neutrophils to promote preeclampsia development.Cellular & molecular immunology · 2021Article
- Management of lung disease in alpha-1 antitrypsin deficiency: what we do and what we do not know.Therapeutic advances in chronic disease · 2021Review
- Translational Clinical Strategies for the Prevention of Gastrointestinal Tract GraftFrontiers in immunology · 2021Review
- Fibrinolytic Serine Proteases, Therapeutic Serpins and Inflammation: Fire Dancers and Firestorms.Frontiers in cardiovascular medicine · 2021Review
- Alpha-1 Antitrypsin Deficiency: a Rare Disease?Current allergy and asthma reports · 2020Review
- Targeting Signal 3 Extracellularly and Intracellularly in Graft-Versus-Host Disease.Frontiers in immunology · 2020Review
- Usefulness of gene expression profiling of bronchoalveolar lavage cells in acute lung allograft rejection.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2019Article
- Article
- Alpha-1 Antitrypsin Substitution for Extrapulmonary Conditions in Alpha-1 Antitrypsin Deficient Patients.Chronic obstructive pulmonary diseases (Miami, Fla.) · 2018Article
- Alpha-1-antitrypsin in cell and organ transplantation.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2018Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Interleukin (IL)-32 was originally identified in natural killer cells and IL-2-activated human T lymphocytes. As T cells are activated in allogeneic transplantation, we determined the role of IL-32 in human mixed lymphocyte cultures (MLCs) and GVHD. In allogeneic MLCs, IL-32 increased two-fold in responding T cells, accompanied by five-fold increases of TNFα, IL-6, and IL-8. After allogeneic hematopoietic cell transplantation, IL-32 mRNA levels in blood leukocytes were statistically significantly higher in patients with acute GVHD (n = 10) than in serial samples from patients who did not develop acute GVHD (n = 5; P = .02). No significant changes in IL-32 levels were present in patients with treated (n = 14) or untreated (n = 8) chronic GVHD, compared with healthy controls (n = 8; P = .5, and P = .74, respectively). As IL-32 is activated by proteinase-3 (PR3), we determined the effect of the serine protease inhibitor α-1 antitrypsin (AAT) on IL-32 levels and showed suppression of IL-32 and T-lymphocyte proliferation in MLCs. In an MHC-minor antigen disparate murine transplant model, preconditioning and postconditioning treatment with AAT resulted in attenuation or prevention of GVHD and superior survival compared with albumin-treated controls (80% vs 44%; P = .04). These findings suggest that AAT modulates immune and inflammatory functions and may represent a novel approach to prevent or treat GVHD.
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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.