ArticleImmunology letters2012
Dispensable role for 4-1BB and 4-1BBL in development of vaccinia virus-specific CD8 T cells.
Article in Immunology letters, 2012. 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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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Commensal bacteria contribute to insulin resistance in aging by activating innate B1a cells.Science translational medicine · 2018Article
- Aging Converts Innate B1a Cells into Potent CD8+ T Cell Inducers.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Transcriptomic analysis of global changes in cytokine expression in mouse spleens following acute Toxoplasma gondii infection.Parasitology research · 2016Article
- 4-1BB Agonists: Multi-Potent Potentiators of Tumor Immunity.Frontiers in oncology · 2015Review
- Article
- The TNF family in T cell differentiation and function--unanswered questions and future directions.Seminars in immunology · 2014Review
- Anatomically restricted synergistic antiviral activities of innate and adaptive immune cells in the skin.Cell host & microbe · 2013Article
- Article
- The death receptor 3/TL1A pathway is essential for efficient development of antiviral CD4⁺ and CD8⁺ T-cell immunity.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2012Article
- Targeting 4-1BB (CD137) to enhance CD8 T cell responses with poxviruses and viral antigens.Frontiers in immunology · 2012Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
CD8 T cells are strongly induced in response to certain strains of vaccinia virus (VACV) and the generation of this population is tightly regulated by two Tumor Necrosis Factor (TNF)/TNFR superfamily members, OX40 (CD134) and CD27. In this study, we examined the role of another member of the TNFR superfamily, 4-1BB (CD137, TNFRSF9), and its ligand (4-1BBL, CD137L, TNFSF9), that have been described to control the generation of memory CD8 T cell populations elicited by other viruses such as influenza. Expression of 4-1BB and 4-1BBL was observed in wild-type mice during the primary infection, but we found that both 4-1BB and 4-1BBL deficient mice generated normal numbers of VACV-specific effector CD8 T cells that produced IFN-γ and TNF. Additionally, CD8 T cells deficient in 4-1BB were able to expand and persist comparably to wild-type T cells in response to VACV infection. Furthermore, the knockout mice also showed no defect in development of VACV-specific CD8 memory T cell populations. Lastly, showing alternate control mechanisms were not active in the gene-deficient environments that masked any activity, blocking 4-1BB/4-1BBL interactions using neutralizing antibody also had no effect on the number of VACV-specific memory CD8 T cells induced. Thus, our data demonstrate that 4-1BB and 4-1BBL do not play a strong or dominant role in driving the generation of high frequencies of VACV-specific CD8 T cells.
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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.