ArticleJournal of virology2009
MyD88 intrinsically regulates CD4 T-cell responses.
Article in Journal of virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
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Who cites it
34 citing papers in PubMed, 47 citations in OpenAlex.
- Myeloid MyD88 restricts CD8Scientific reports · 2023Article
- Foreign body response to synthetic polymer biomaterials and the role of adaptive immunity.Biomedical materials (Bristol, England) · 2022Review
- Toll-like Receptors in Viral Encephalitis.Viruses · 2021Review
- MAP3K2 augments Th1 cell differentiation via IL-18 to promote T cell-mediated colitis.Science China. Life sciences · 2021Article
- Mitochondrial Fission Factor Is a Novel Interacting Protein of the Critical B Cell Survival Regulator TRAF3 in B Lymphocytes.Frontiers in immunology · 2021Article
- Elevated Choline Kinase α-Mediated Choline Metabolism Supports the Prolonged Survival of TRAF3-Deficient B Lymphocytes.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- ST2/MyD88 Deficiency Protects Mice against Acute Graft-versus-Host Disease and Spares Regulatory T Cells.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- MyD88 Signaling in T Cells Is Critical for Effector CD4 T Cell Differentiation following a Transitional T Follicular Helper Cell Stage.Infection and immunity · 2018Article
- MyD88 in antigen-presenting cells is not required for CD4+ T-cell responses during peptide nanofiber vaccination.MedChemComm · 2018Article
- Article
- Neutralizing Antibody Responses to Viral Infections Are Linked to the Non-classical MHC Class II Gene H2-Ob.Immunity · 2017Article
- A distinct brain pathway links viral RNA exposure to sickness behavior.Scientific reports · 2016Article
- Signaling mechanisms of bortezomib in TRAF3-deficient mouse B lymphoma and human multiple myeloma cells.Leukemia research · 2016Article
- Recipient Myd88 Deficiency Promotes Spontaneous Resolution of Kidney Allograft Rejection.Journal of the American Society of Nephrology : JASN · 2015Article
- Augmentation of transgene-encoded protein after neonatal injection of adeno-associated virus improves hepatic copy number without immune responses.Pediatric research · 2015Article
- STING-dependent cytosolic DNA sensing mediates innate immune recognition of immunogenic tumors.Immunity · 2014Article
- Mutated in colorectal cancer (MCC) is a novel oncogene in B lymphocytes.Journal of hematology & oncology · 2014Article
- MyD88-dependent immunity to a natural model of vaccinia virus infection does not involve Toll-like receptor 2.Journal of virology · 2014Article
- Expression and function of a novel isoform of Sox5 in malignant B cells.Leukemia research · 2014Article
- N-benzyladriamycin-14-valerate (AD 198) exhibits potent anti-tumor activity on TRAF3-deficient mouse B lymphoma and human multiple myeloma.BMC cancer · 2013Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Myeloid differentiation factor 88 (MyD88) is an essential adaptor protein in the Toll-like receptor-mediated innate signaling pathway, as well as in interleukin-1 receptor (IL-1R) and IL-18R signaling. The importance of MyD88 in the regulation of innate immunity to microbial pathogens has been well demonstrated. However, its role in regulating acquired immunity to viral pathogens and neuropathogenesis is not entirely clear. In the present study, we examine the role of MyD88 in the CD4(+) T-cell response following lymphocytic choriomeningitis virus (LCMV) infection. We demonstrate that wild-type (WT) mice developed a CD4(+) T-cell-mediated wasting disease after intracranial infection with LCMV. In contrast, MyD88 knockout (KO) mice did not develop wasting disease in response to the same infection. This effect was not the result of MyD88 regulation of IL-1 or IL-18 responses since IL-1R1 KO and IL-18R KO mice were not protected from weight loss. In the absence of MyD88, naïve CD4(+) T cells failed to differentiate to LCMV-specific CD4 T cells. We demonstrated that MyD88 KO antigen-presenting cells are capable of activating WT CD4(+) T cells. Importantly, when MyD88 KO CD4(+) T cells were reconstituted with an MyD88-expressing lentivirus, the rescued CD4(+) T cells were able to respond to LCMV infection and support IgG2a antibody production. Overall, these studies reveal a previously unknown role of MyD88-dependent signaling in CD4(+) T cells in the regulation of the virus-specific CD4(+) T-cell response and in viral infection-induced immunopathology in the central nervous system.
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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.