ArticleBlood2011
Antiviral memory CD8 T-cell differentiation, maintenance, and secondary expansion occur independently of MyD88.
Article in Blood, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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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.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- Regulatory T cell-derived IL-1Ra suppresses the innate response to respiratory viral infection.Nature immunology · 2023Article
- Myeloid MyD88 restricts CD8Scientific reports · 2023Article
- p53 Hinders CRISPR/Cas9-Mediated Targeted Gene Disruption in Memory CD8 T Cells In Vivo.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- MyD88 Shapes Vaccine Immunity by Extrinsically Regulating Survival of CD4+ T Cells during the Contraction Phase.PLoS pathogens · 2016Article
- Regulatory T cell expressed MyD88 is critical for prolongation of allograft survival.Transplant international : official journal of the European Society for Organ Transplantation · 2016Article
- ST2 contributes to T-cell hyperactivation and fatal hemophagocytic lymphohistiocytosis in mice.Blood · 2016Article
- Recipient Myd88 Deficiency Promotes Spontaneous Resolution of Kidney Allograft Rejection.Journal of the American Society of Nephrology : JASN · 2015Article
- Microbiota signalling through MyD88 is necessary for a systemic neutrophilic inflammatory response.Immunology · 2013Article
- MyD88 is essential to sustain mTOR activation necessary to promote T helper 17 cell proliferation by linking IL-1 and IL-23 signaling.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Arenavirus evasion of host anti-viral responses.Viruses · 2012Review
- Regulation of B-cell responses by Toll-like receptors.Immunology · 2012Review
- TLR9 and MyD88 are crucial for the development of protective immunity to malaria.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Regulation and function of mTOR signalling in T cell fate decisions.Nature reviews. Immunology · 2012Review
- Peroxisome proliferator-activated receptor gamma is required for CD4+ T cell-mediated lymphopenia-associated autoimmunity.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- CD8(+) T cells: foot soldiers of the immune system.Immunity · 2011Review
- Article
- Innate Immune Responses to AAV Vectors.Frontiers in microbiology · 2011Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Inflammatory signals induced during infection regulate T-cell expansion, differentiation, and memory formation. Toll-like receptors (TLRs) are inflammatory mediators that allow innate immune cells to recognize and respond to invading pathogens. In addition to their role in innate immune cells, we have found that signals delivered through the TLR adapter protein myeloid differentiation protein 88 (MyD88) play a critical, T cell-intrinsic role in supporting the survival and accumulation of antigen-specific effector cells after acute viral infection. However, the importance of MyD88-dependent signals in regulating the generation and maintenance of memory T cells remained unclear. To address this, we used a novel, inducible knockout system to examine whether MyD88 is required for optimal memory CD8 T-cell generation and responses after lymphocytic choriomeningitis virus infection. We show that whereas MyD88 is critical for initial T-cell expansion, it is not required for the subsequent differentiation and stable maintenance of a memory T-cell population. Furthermore, in contrast to naive CD8 T cells, memory CD8 T cells do not depend on MyD88 for their secondary expansion. Our findings clarify the importance of MyD88 during distinct phases of the antiviral T-cell response and establish differential dependence on MyD88 signaling as a novel characteristic that distinguishes naive from memory CD8 T cells.
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What OpenQuestion holds
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.