ArticleGastroenterology2010
Pathogenic and protective roles of MyD88 in leukocytes and epithelial cells in mouse models of inflammatory bowel disease.
Article in Gastroenterology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 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
61 citing papers in PubMed, 105 citations in OpenAlex.
- Specialized Dendritic Cells Mediating Peripheral Tolerance to Intestinal Antigens.Immunological reviews · 2026Review
- TLR4/MyD88 expression patterns and novel genetic variants: association with aggressive clinicopathological features in colorectal cancer.Frontiers in oncology · 2025Article
- The inflammatory response to birth requires MyD88 and is driven by both mother and offspring.Brain, behavior, and immunity · 2024Article
- Gut microbiota and atopic dermatitis: a two-sample Mendelian randomization study.Frontiers in medicine · 2023Article
- Know your neighbors: microbial recognition at the intestinal barrier and its implications for gut homeostasis and inflammatory bowel disease.Frontiers in cell and developmental biology · 2023Review
- Pattern Recognition Receptor Signaling and Cytokine Networks in Microbial Defenses and Regulation of Intestinal Barriers: Implications for Inflammatory Bowel Disease.Gastroenterology · 2022Review
- Challenges and opportunities targeting mechanisms of epithelial injury and recovery in acute intestinal graft-versus-host disease.Mucosal immunology · 2022Review
- Microbial signals, MyD88, and lymphotoxin drive TNF-independent intestinal epithelial tissue damage.The Journal of clinical investigation · 2022Article
- Article
- Inflammatory Bowel Disease Therapeutics: A Focus on Probiotic Engineering.Mediators of inflammation · 2022Review
- Cell Wall Contents of Probiotics (Lactobacillus species) Protect Against Lipopolysaccharide (LPS)-Induced Murine Colitis by Limiting Immuno-inflammation and Oxidative Stress.Probiotics and antimicrobial proteins · 2021Article
- Evaluation of E. coli Nissle1917 derived metabolites in modulating key mediator genes of the TLR signaling pathway.BMC research notes · 2021Article
- Opposing effects of antibiotics and germ-free status on neuropeptide systems involved in social behaviour and pain regulation.BMC neuroscience · 2020Article
- Gut Microbiota and Intestinal Epithelial Myd88 Signaling Are Crucial for Renal Injury in UUO Mice.Frontiers in immunology · 2020Article
- Host Factors of Favorable Intestinal Microbial Colonization.Frontiers in immunology · 2020Review
- Crosstalk Between Gut Microbiota and Innate Immunity and Its Implication in Autoimmune Diseases.Frontiers in immunology · 2020Review
- Keep calm: the intestinal barrier at the interface of peace and war.Cell death & disease · 2019Review
- Macrophage/microglial Ezh2 facilitates autoimmune inflammation through inhibition of Socs3.The Journal of experimental medicine · 2018Article
- Human ALPI deficiency causes inflammatory bowel disease and highlights a key mechanism of gut homeostasis.EMBO molecular medicine · 2018Article
- Critical Role of Alternative M2 Skewing in miR-155 Deletion-Mediated Protection of Colitis.Frontiers in immunology · 2018Article
1 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
BACKGROUND &
aimsToll-like receptors (TLR) are innate immune receptors involved in recognition of the intestinal microflora; they are expressed by numerous cell types in the intestine, including epithelial cells, myeloid cells, and lymphocytes. Little is known about the relative contributions of TLR signaling in distinct cellular compartments to intestinal homeostasis. We aimed to define the roles of TLR signals in distinct cell types in the induction and regulation of chronic intestinal inflammation.
methodsWe assessed the roles of the shared TLR signaling adaptor protein, MyD88, in several complementary mouse models of inflammatory bowel disease, mediated by either innate or adaptive immune activation. MyD88-deficient mice and bone marrow chimeras were used to disrupt TLR signals selectively in distinct cellular compartments in the intestine.
resultsMyD88-dependent activation of myeloid cells was required for the development of chronic intestinal inflammation. By contrast, although epithelial cell MyD88 signals were required for host survival, they were insufficient to induce intestinal inflammation in the absence of an MyD88-competent myeloid compartment. MyD88 expression by T cells was not required for their pathogenic and regulatory functions in the intestine.
conclusionsCellular compartmentalization of MyD88 signals in the intestine allow the maintenance of host defense and prevent deleterious inflammatory responses.
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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.