ArticleArteriosclerosis, thrombosis, and vascular biology2014
Bim regulates alloimmune-mediated vascular injury through effects on T-cell activation and death.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 9 citations in OpenAlex.
- Improving the Rigor and Reproducibility of Flow Cytometry-Based Clinical Research and Trials Through Automated Data Analysis.Cytometry. Part A : the journal of the International Society for Analytical Cytology · 2020Article
- Disruption of the Gut Microbiota With Antibiotics Exacerbates Acute Vascular Rejection.Transplantation · 2018Article
- [Study on the expression of T, B lymphocyte antigen and platelet antibodies in patients with platelet transfusion refractoriness].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2016Article
- Mouse model of alloimmune-induced vascular rejection and transplant arteriosclerosis.Journal of visualized experiments : JoVE · 2015Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
objectiveBim is a proapoptotic Bcl-2 protein known to downregulate immune responses and to also be required for antigen-induced T-cell activation. However, it is not known how the effect of Bim on these offsetting processes determines the outcome of allogeneic immune responses. We have defined the role of Bim in regulating alloantigen-driven T-cell responses in a model of vascular rejection. APPROACH AND
resultsBim was required for proliferation of CD4 and CD8 T cells, and for interleukin-2 production, in T cells stimulated with alloantigen in vitro. Moreover, a partial reduction in Bim expression was sufficient to attenuate T-cell activation, whereas a complete elimination of Bim was required to prevent CD4 T-cell death in response to cytokine withdrawl. When alloimmune-mediated vascular rejection was examined using an aortic interposition model, there was significantly less intimal thickening in Bim(+/-), but not Bim(-/-), graft recipients. T-cell proliferation in response to allograft arteries was significantly reduced in both Bim(+/-) and Bim(-/-) mice, but cell death was attenuated only in Bim(-/-) animals.
conclusionsBim controls both T-cell activation and death in response to alloantigen stimulation. These processes act cooperatively to determine the outcome of immune responses in allograft arteries.
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