ArticleInnate immunity2014
MyD88 mediates the decision to die by apoptosis or necroptosis after UV irradiation.
Article in Innate immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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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.
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Who cites it
22 citing papers in PubMed, 39 citations in OpenAlex.
- MyD88 determines T cell fate through BCAP-PI3K signaling.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Innate Immune Sensors and Cell Death-Frontiers Coordinating Homeostasis, Immunity, and Inflammation in Skin.Viruses · 2025Review
- Full-length GSDME mediates pyroptosis independent from cleavage.Nature cell biology · 2024Article
- Mediators of necroptosis: from cell death to metabolic regulation.EMBO molecular medicine · 2024Review
- Role of DAMPs and cell death in autoimmune diseases: the example of multiple sclerosis.Genes and immunity · 2023Review
- Cooperative effects of RIG-I-like receptor signaling and IRF1 on DNA damage-induced cell death.Cell death & disease · 2022Article
- The cytotoxicity and apoptotic effects of verbascoside on breast cancer 4T1 cell line.BMC pharmacology & toxicology · 2021Article
- [Effect of ultraviolet irradiation on the proliferation of acute promyelocytic leukemia cells under hypoxic conditions and related mechanisms].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2019Article
- Protective Effect of Baicalin Against TLR4-mediated UVA-induced Skin Inflammation.Photochemistry and photobiology · 2019Article
- Article
- Two-in-one: UV radiation simultaneously induces apoptosis and NETosis.Cell death discovery · 2018Article
- From Early Immunomodulatory Triggers to Immunosuppressive Outcome: Therapeutic Implications of the Complex Interplay Between the Wavebands of Sunlight and the Skin.Frontiers in medicine · 2018Review
- Human and Murine Evidence for Mechanisms Driving Autoimmune Photosensitivity.Frontiers in immunology · 2018Review
- Pattern Recognition Receptors and the Host Cell Death Molecular Machinery.Frontiers in immunology · 2018Review
- Ebola virus glycoprotein directly triggers T lymphocyte death despite of the lack of infection.PLoS pathogens · 2017Article
- Pericyte MyD88 and IRAK4 control inflammatory and fibrotic responses to tissue injury.The Journal of clinical investigation · 2017Article
- Necroptosis in tumorigenesis, activation of anti-tumor immunity, and cancer therapy.Oncotarget · 2016Review
- Inhibition of regulated cell death by cell-penetrating peptides.Cellular and molecular life sciences : CMLS · 2016Review
- Regulation of necrotic cell death: p53, PARP1 and cyclophilin D-overlapping pathways of regulated necrosis?Cellular and molecular life sciences : CMLS · 2016Review
- Baicalin Protects Keratinocytes from Toll-like Receptor-4 Mediated DNA Damage and Inflammation Following Ultraviolet Irradiation.Photochemistry and photobiology · 2015Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
UV irradiation-induced cellular damage is classically associated with apoptosis and is known to result in systemic immunosuppression. How the decision to undergo apoptosis is made following UV is not fully understood. We hypothesize that a central mediator of TLR signaling, MyD88, determines cell fate after UV exposure. Survival after UV of immortalized bone marrow-derived macrophages (BMDM) and ex vivo peritoneal macrophages (PM) from MyD88 germline-deficient mice (MyD88(-/-)) was significantly higher than wild type (WT) PM. UV-induced apoptosis (DNA laddering) in PM and epidermis of MyD88(-/-) animals versus WT was decreased. In MyD88(-/-) PM, decreased cleavage of caspase 3, as well as pro-necroptotic protein, RIP1, and a significant increase in transcription and release of pro-inflammatory TNF-α, suggest that necroptosis, rather than apoptosis, has been initiated. In vivo studies confirm this hypothesis after UV, showing low apoptosis by TUNEL and inflammation in MyD88(-/-) skin sections. Considering that MyD88 participates in many TLR pathways, BMDM from TLR2(-/-), TLR4(-/-) and WT mice were compared for evidence of UV-induced apoptosis. Only TLR4(-/-) BMDM and PM had a similar phenotype to MyD88(-/-), suggesting that the TLR4-MyD88 axis importantly contributes to cell fate decision. Our study describes a new cellular consequence of MyD88 signaling after UV, and may provide rationale for therapies to mitigate UV-induced immunosuppression.
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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.