ArticleJournal of immunology (Baltimore, Md. : 1950)2016
CD8+ Effector T Cell Migration to Pancreatic Islet Grafts Is Dependent on Cognate Antigen Presentation by Donor Graft Cells.
Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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
8 citing papers in PubMed, 9 citations in OpenAlex.
- NEUROD1 reinforces endocrine cell fate acquisition in pancreatic development.Nature communications · 2023Article
- Multi-functional adaptor SKAP1: regulator of integrin activation, the stop-signal, and the proliferation of T cells.Frontiers in immunology · 2023Review
- Treg suppression of immunity within inflamed allogeneic grafts.JCI insight · 2022Article
- Single-Cell Landscape of Mouse Islet Allograft and Syngeneic Graft.Frontiers in immunology · 2022Article
- Cross-dressed dendritic cells sustain effector T cell responses in islet and kidney allografts.The Journal of clinical investigation · 2020Article
- Quantifying in situ adaptive immune cell cognate interactions in humans.Nature immunology · 2019Article
- Integrins in T Cell Physiology.International journal of molecular sciences · 2018Review
- Evolving Approaches in the Identification of Allograft-Reactive T and B Cells in Mice and Humans.Transplantation · 2017Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 4 countries.
Funding
Abstract
Pancreatic islet transplantation is a promising therapy for diabetes, but acute rejection of the islets by host effector T cells has hindered clinical application. In this study, we addressed the mechanisms of CD8(+) effector T cell migration to islet grafts because interrupting this step is key to preventing rejection. We found that effector T cell migration to revascularized islet transplants in mice is dependent on non-self Ag recognition rather than signaling via Gαi-coupled chemokine receptors. Presentation of non-self Ag by donor cells was necessary for migration, whereas Ag presentation by recipient cells was dispensable. We also observed that deficiency of SKAP1, an immune cell adaptor downstream of the TCR and important for integrin activation, prolongs allograft survival but does not reduce effector T cell migration to the graft. Therefore, effector T cell migration to transplanted islets is Ag driven, not chemokine driven, but SKAP1 does not play a critical role in this process.
Indexed as
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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.