ArticleBlood2013
FANCA and FANCC modulate TLR and p38 MAPK-dependent expression of IL-1β in macrophages.
Article in Blood, 2013. 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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Who cites it
22 citing papers in PubMed, 32 citations in OpenAlex.
- Distinct developmental outcomes in DNA repair-deficient FANCC c.67delG mutant and FANCCCell death and differentiation · 2025Article
- Inflammatory pathways and the bone marrow microenvironment in inherited bone marrow failure syndromes.Stem cells (Dayton, Ohio) · 2025Review
- RUNX1 mutations mitigate quiescence to promote transformation of hematopoietic progenitors in Fanconi anemia.Leukemia · 2023Article
- Transforming growth factor-β signaling modifies the hematopoietic acute inflammatory response to drive bone marrow failure.Haematologica · 2022Article
- N6-methylandenosine-related immune genes correlate with prognosis and immune landscapes in gastric cancer.Frontiers in oncology · 2022Article
- Zika virus depletes neural stem cells and evades selective autophagy by suppressing the Fanconi anemia protein FANCC.EMBO reports · 2020Article
- An induced pluripotent stem cell model of Fanconi anemia reveals mechanisms of p53-driven progenitor cell differentiation.Blood advances · 2020Article
- Canonical and Noncanonical Roles of Fanconi Anemia Proteins: Implications in Cancer Predisposition.Cancers · 2020Review
- Effects of steroidal saponins extract from Ophiopogon japonicus root ameliorates doxorubicin-induced chronic heart failure by inhibiting oxidative stress and inflammatory response.Pharmaceutical biology · 2019Article
- Natural Killer Cell Degranulation Defect: A Cause for Impaired NK-Cell Cytotoxicity and Hyperinflammation in Fanconi Anemia Patients.Frontiers in immunology · 2019Article
- Article
- Recent advances in understanding hematopoiesis in Fanconi Anemia.F1000Research · 2018Review
- Recent insights into the molecular basis of Fanconi anemia: genes, modifiers, and drivers.International journal of hematology · 2017Review
- Emerging functions of the Fanconi anemia pathway at a glance.Journal of cell science · 2017Review
- Loss of the homologous recombination geneProceedings of the National Academy of Sciences of the United States of America · 2017Article
- Endogenous DNA Damage Leads to p53-Independent Deficits in Replicative Fitness in Fetal Murine Fancd2Stem cell reports · 2016Article
- Article
- Cytokine overproduction and crosslinker hypersensitivity are unlinked in Fanconi anemia macrophages.Journal of leukocyte biology · 2016Article
- Toll-like receptor signaling in hematopoietic homeostasis and the pathogenesis of hematologic diseases.Frontiers of medicine · 2015Review
- Engagement of Toll-like receptor 2 enhances interleukin (IL)-17(+) autoreactive T cell responses via p38 mitogen-activated protein kinase signalling in dendritic cells.Clinical and experimental immunology · 2014Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Hematopoietic stem and progenitor cells with inactivated Fanconi anemia (FA) genes, FANCA and FANCC, are hypersensitive to inflammatory cytokines. One of these, tumor necrosis factor α (TNF-α), is also overproduced by FA mononuclear phagocytes in response to certain Toll-like receptor (TLR) agonists, creating an autoinhibitory loop that may contribute to the pathogenesis of progressive bone marrow (BM) failure and selection of TNF-α-resistant leukemic stem cell clones. In macrophages, the TNF-α overproduction phenotype depends on p38 mitogen-activated protein kinase (MAPK), an enzyme also known to induce expression of other inflammatory cytokines, including interleukin 1β (IL-1β). Reasoning that IL-1β might be involved in a like autoinhibitory loop, we determined that (1) TLR activation of FANCA- and FANCC-deficient macrophages induced overproduction of both TNF-α and IL-1β in a p38-dependent manner; (2) exposure of Fancc-deficient BM progenitors to IL-1β potently suppressed the expansion of multipotent progenitor cells in vitro; and (3) although TNF-α overexpression in FA cells is controlled posttranscriptionally by the p38 substrate MAPKAPK-2, p38-dependent overproduction of IL-1β is controlled transcriptionally. We suggest that multiple inflammatory cytokines overproduced by FANCA- and FANCC-deficient mononuclear phagocytes may contribute to the progressive BM failure that characterizes FA, and that to achieve suppression of this proinflammatory state, p38 is a more promising molecular therapeutic target than either IL-1β or TNF-α alone.
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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.