ArticleAmerican journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons2015
Rapamycin ameliorates the CTLA4-Ig-mediated defect in CD8(+) T cell immunity during gammaherpesvirus infection.
Article in American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The trial behind it
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- CD154:CD11b blockade enhances CD8+ T cell differentiation during infection but not transplantation.JCI insight · 2025Article
- mTOR Deletion Alleviates CD4+ T-Cell Dysfunction in Sepsis through Reducing CTLA4 Accumulation Mediated by Rescuing Autophagy.Mediators of inflammation · 2024Article
- Evaluation and mechanism study of Pien Tze Huang against EV-A71 infection.Frontiers in pharmacology · 2023Article
- Monoclonal Antibody-Based Therapies for Myasthenia Gravis.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2020Review
- Insights into CD8 T Cell Activation and Exhaustion from a Mouse Gammaherpesvirus Model.Viral immunology · 2020Review
- CTLA4Ig-based T-cell costimulation blockade is associated with reduction of adenovirus viremia following post-transplantation cyclophosphamide-based haploidentical transplantation.Bone marrow transplantation · 2020Article
- Advances in autoimmune myasthenia gravis management.Expert review of neurotherapeutics · 2018Review
- Production of interleukin-1β related to mammalian target of rapamycin/Toll-like receptor 4 signaling pathway duringInternational journal of ophthalmology · 2018Article
- Drug Modulators of B Cell Signaling Pathways and Epstein-Barr Virus Lytic Activation.Journal of virology · 2017Article
- New perspectives on mTOR inhibitors (rapamycin, rapalogs and TORKinibs) in transplantation.British journal of clinical pharmacology · 2016Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Latent viral infections are a major concern among immunosuppressed transplant patients. During clinical trials with belatacept, a CTLA4-Ig fusion protein, patients showed an increased risk of Epstein-Barr virus-associated posttransplant lymphoproliferative disorder, thought to be due to a deficient primary CD8(+) T cell response to the virus. Using a murine model of latent viral infection, we observed that rapamycin treatment alone led to a significant increase in virus-specific CD8(+) T cells, as well as increased functionality of these cells, including the ability to make multiple cytokines, while CTLA4-Ig treatment alone significantly dampened the response and inhibited the generation of polyfunctional antigen-specific CD8(+) T cells. However, the addition of rapamycin to the CTLA4-Ig regimen was able to quantitatively and qualitatively restore the antigen-specific CD8(+) T cell response to the virus. This improvement was physiologically relevant, in that CTLA4-Ig treated animals exhibited a greater viral burden following infection that was reduced to levels observed in untreated immunocompetent animals by the addition of rapamycin. These results reveal that modulation of T cell differentiation though inhibition of mTOR signaling can restore virus-specific immune competence even in the absence of CD28 costimulation, and have implications for improving protective immunity in transplant recipients.
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