ArticleThe American journal of pathology1998
Pattern of graft- and host-specific MHC class II expression in long-term murine cardiac allografts: origin of inflammatory and vascular wall cells.
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 14 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
14 citing papers in PubMed, 55 citations in OpenAlex.
- STEMIN and YAP5SA synthetic modified mRNAs regenerate and repair infarcted mouse hearts.The journal of cardiovascular aging · 2022Article
- Major histocompatibility complexes are up-regulated in glomerular endothelial cells via activation of c-Jun N-terminal kinase in 5/6 nephrectomy mice.British journal of pharmacology · 2020Article
- A Novel Model on DST-Induced Transplantation Tolerance by the Transfer of Self-Specific Donor tTregs to a Haplotype-Matched Organ Recipient.Frontiers in immunology · 2017Article
- Diversity of the CD4 T Cell Alloresponse: The Short and the Long of It.Cell reports · 2016Article
- Immune-mediated vascular injury and dysfunction in transplant arteriosclerosis.Frontiers in immunology · 2014Review
- Antibodies in transplantation: the effects of HLA and non-HLA antibody binding and mechanisms of injury.Methods in molecular biology (Clifton, N.J.) · 2013Article
- Genetic or pharmaceutical blockade of phosphoinositide 3-kinase p110δ prevents chronic rejection of heart allografts.PloS one · 2012Article
- Simvastatin does not prevent acute cardiac allograft rejection in CD28-deficient mice.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2009Article
- A two-step model of acute CD4 T-cell mediated cardiac allograft rejection.Journal of immunology (Baltimore, Md. : 1950) · 2004Article
- Stem cell origins of intimal cells in graft arterial disease.Current atherosclerosis reports · 2003Review
- Vascular smooth muscle cells of recipient origin mediate intimal expansion after aortic allotransplantation in mice.The American journal of pathology · 2001Article
- Origin of neointimal endothelium and alpha-actin-positive smooth muscle cells in transplant arteriosclerosis.The Journal of clinical investigation · 2001Article
- Association of B7-1 co-stimulation with the development of graft arterial disease. Studies using mice lacking B7-1, B7-2, or B7-1/B7-2.The American journal of pathology · 2000Article
- Donor MHC and adhesion molecules in transplant arteriosclerosis.The Journal of clinical investigation · 1999Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
In solid-tissue allografts, donor vascular cells as well as recipient inflammatory cells can express MHC class II molecules. However, it is uncertain how much residual donor endothelium persists and to what extent donor versus recipient MHC class II expression can contribute to the ongoing immune response, especially in long-term grafts. To establish the origin of class-II-expressing cells in the allograft, we evaluated the expression of donor- or recipient-specific MHC class II molecules in murine cardiac allografts. Donor hearts from BALB/c (H-2d) mice were transplanted into C57BL/6 (B6, H-2b) recipients; B6 isografts served as controls. Untreated allografts ceased functioning at approximately 7 days with severe parenchymal rejection. Allografts from recipients treated with anti-CD4 and anti-CD8 MAbs after transplantation were explanted at 8 to 12 weeks and demonstrated intimal fibroproliferative lesions with a mild parenchymal mononuclear cell infiltrate. Class II expression in isografts was limited to epicardial macrophages. Both acutely rejecting and long-term allografts contained abundant macrophages expressing recipient class II molecules. Occasional cells (passenger leukocytes) in untreated, acutely rejecting allografts bore donor class II molecules; long-term allografts contained few such cells. In contrast, vascular endothelial and medial smooth muscle cells consistently expressed donor class II molecules. These results suggest that ongoing MHC class II expression in donor vascular cells, as well as in recipient macrophages, may contribute to sustained activation of host T cells with consequent release of cytokines that ultimately promote the development of graft arteriosclerosis.
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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.