ArticleJournal of clinical immunology2007
Apoptosis inhibitor expressed by macrophages tempers autoimmune colitis and the risk of colitis-based carcinogenesis in TCRalpha-/- mice.
Article in Journal of clinical immunology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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
2 citing papers in PubMed, 9 citations in OpenAlex.
- Administration of an antibody against apoptosis inhibitor of macrophage prevents aortic aneurysm progression in mice.Scientific reports · 2024Article
- Apoptosis inhibitor of macrophage as a biomarker for disease activity in Japanese children with IgA nephropathy and Henoch-Schönlein purpura nephritis.Pediatric research · 2021Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCrohn's disease and ulcerative colitis (UC) are the two main entities involved in human inflammatory bowel disease (IBD). However, their precise etiologies remain unclear. To study the development of mucosal inflammation, and chronic inflammation-based dysplasia and carcinoma formation, we examined possible roles of the apoptosis inhibitor expressed by macrophages (AIM) in an experimental IBD model.
methodsIn this study, we used T cell receptor alpha deficient (TCRalpha(-/-)) mice, a known UC-like colitis model. We generated TCRalpha(-/-) x AIM(-/-) double knockout mice by crossbreeding TCRalpha(-/-) with AIM(-/-) mice. At 24 weeks of age, mice were killed to obtain colon tissues for pathological examinations. TCRalpha(-/-) x AIM(+/-) mice, heterozygous littermates of TCRalpha(-/-) x AIM(-/-) mice, were used as controls.
resultsSevere colitis was observed in TCRalpha(-/-) x AIM(-/-) mice, when compared with TCRalpha(-/-) x AIM(+/-) mice. Dysplasia was detected in TCRalpha(-/-) x AIM(-/-) mice, but not in TCRalpha(-/-) x AIM(+/-) mice. Adenocarcinoma formation was observed from dysplasia only in TCRalpha(-/-) x AIM(-/-) mice.
conclusionNot only a high incidence of severe colitis but also dysplasia and adenocarcinoma formation were observed in TCRalpha(-/-) x AIM(-/-) mice only. AIM have some regulatory roles in inflammation and progression of dysplasia to carcinoma in TCRalpha(-/-) mice.
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