ArticleImmunology2010
Toll-like receptor-induced innate immune responses in non-parenchymal liver cells are cell type-specific.
Article in Immunology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 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
108 citing papers in PubMed, 208 citations in OpenAlex.
- Dietary, Nutrient, and Supramolecular Nanofiber Modulation of the Liver Sinusoidal Clearance System in Metabolic Diseases and Aging.Biomedicines · 2026Review
- Toll Like Receptor 4: A Potential Link Between Obesity and Metabolic Diseases.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2026Review
- Immune cells in liver transplantation: Dual roles, mechanistic insights, and targeted therapeutic strategies.Immunologic research · 2026Review
- Gut-liver axis molecular mechanisms in alcohol-associated liver disease.Alcohol (Fayetteville, N.Y.) · 2026Review
- 3D co-cultures of primary human hepatocytes and Kupffer-like cells to address innate immune responses to rAAV.Scientific reports · 2025Article
- Liver immunology: Biological role and clinical significance.World journal of hepatology · 2025Review
- Hepatocyte Toll-like receptors contribute to the hepcidin inflammatory response to pathogens and pathogen-derived ligands.HemaSphere · 2025Article
- Research Progress on the Immune Function of Liver Sinusoidal Endothelial Cells in Sepsis.Cells · 2025Review
- Review
- Review
- Systemic mechanisms of necrotic cell debris clearance.Cell death & disease · 2024Review
- Role of liver sinusoidal endothelial cell in metabolic dysfunction-associated fatty liver disease.Cell communication and signaling : CCS · 2024Review
- Fetal liver development and implications for liver disease pathogenesis.Nature reviews. Gastroenterology & hepatology · 2023Review
- Evaluation of drug-induced liver toxicity of trovafloxacin and levofloxacin in a human microphysiological liver model.Scientific reports · 2023Article
- Angiocrine Signaling in Sinusoidal Health and Disease.Seminars in liver disease · 2023Review
- Endotheliopathy in the metabolic syndrome: Mechanisms and clinical implications.Pharmacology & therapeutics · 2023Review
- Toll- like receptor 2 polymorphism and IL-6 profile in relation to disease progression in chronic HBV infection: a case control study in Egyptian patients.Clinical and experimental medicine · 2023Article
- Vascularized Tissue Organoids.Bioengineering (Basel, Switzerland) · 2023Review
- The multifaceted role of macrophages during acute liver injury.Frontiers in immunology · 2023Review
- Interorgan communication with the liver: novel mechanisms and therapeutic targets.Frontiers in immunology · 2023Review
48 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Little is known of how the Toll-like receptor (TLR) system can modulate the function of non-parenchymal liver cells (NPC) as a major component of the innate and adaptive immune system of the liver. To investigate the diversification of TLR signalling pathways in NPC, we isolated Kupffer cells (KC) and liver sinusoidal endothelial cells (LSEC) from wild-type C57BL/6 mice and examined their responses to TLR1 to TLR9 agonists. The data show that KC respond to all TLR ligands by producing tumour necrosis factor-alpha (TNF-alpha) or interleukin-6 (IL-6), to TLR3 and TLR4 ligands only by producing interferon-beta (IFN-beta), to TLR1 and TLR8 ligands by significantly up-regulating major histocompatibility complex (MHC) class II and costimulatory molecules, and to TLR1, -2, -4 and -6 ligands by inducing high levels of T-cell proliferation and IFN-gamma production in the mixed lymphocyte reaction (MLR). Similarly, LSEC respond to TLR1 to -4, -6, -8 and -9 ligands by producing TNF-alpha, to TLR3 and -4 ligands by producing IL-6, and to TLR3 ligands by producing IFN-beta. Interestingly, despite significant up-regulation of MHC class II and co-stimulatory molecules in response to TLR8 ligands, LSEC stimulated by TLR1, -2 or -6 could stimulate allogeneic T cells as assessed by MLR. By contrast, myeloid dendritic cells, used as positive control for classical antigen-presenting cells, respond to TLR1, -2, -4 and -9 ligands by both up-regulation of CD40 and activation of allogeneic T cells. In conclusion, NPC display a restricted TLR-mediated activation profile when compared with 'classical' antigen-presenting cells which may, at least in part, explain their tolerogenic function in the liver.
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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.