ArticleThe American journal of pathology1998
Leukocyte-suppressing influences of interleukin (IL)-10 in cardiac allografts: insights from IL-10 knockout mice.
Article in The American journal of pathology, 1998. 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.
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Who cites it
5 citing papers in PubMed, 36 citations in OpenAlex.
- IL-10 for cardiac autophagy modulation: New direction in the pursuit of perfection.Journal of molecular and cellular cardiology · 2016Article
- Bronchiolitis obliterans syndrome: the Achilles' heel of lung transplantation.Seminars in respiratory and critical care medicine · 2013Review
- Lung transplantation: infection, inflammation, and the microbiome.Seminars in immunopathology · 2011Review
- Cardiac allograft vasculopathy: the Achilles' heel of long-term survival after cardiac transplantation.Current atherosclerosis reports · 2006Review
- Interleukin 10 attenuates neointimal proliferation and inflammation in aortic allografts by a heme oxygenase-dependent pathway.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
To investigate the role of interleukin (IL)-10 in late graft outcomes, we compared BALB/c donor hearts transplanted into immunosuppressed wild-type or IL-10 gene-deficient (-/-) C57BL recipients (n = 49) at 50 +/- 5 days. There was prominent leukocyte infiltration and parenchymal destruction with more severe vascular occlusion in grafts from IL-10 -/- recipients. An occlusive CD45+ arteritis with medial necrosis occurred with IL-10 deficiency instead of the a-smooth muscle actin-rich arteriosclerosis seen in wild-type recipients. Increased interferon (IFN)-gamma as well as Mac-1, inducible nitric oxide synthase, and allograft inflammatory factor-1 (but not CD3 and IL-4) transcript levels were seen in allografts from IL-10 -/- recipients as assessed by 32p reverse transcription polymerase chain reaction. We then evaluated the contribution of IFN-gamma-mediated responses by neutralizing IFN-gamma. Anti-IFN-gamma monoclonal antibody (MAb) treatment of IL-10 -/- recipients did not improve graft survival, parenchymal rejection, or occlusive arteritis, indicating that these processes are IFN-gamma independent. However, medial smooth muscle cell loss in IL-10 -/- recipients was attenuated by anti-IFN-gamma MAb. Hence, in this transplant model, IL-10 suppresses T cell and macrophage responses in the parenchyma and vasculature and confers a protective effect against late rejection.
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