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Littérature scientifique sur le sujet « Endosomal TLRs »

Auteur : Grafiati

Publié le 9 mars 2023

Mis à jour le 31 juillet 2025

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Articles de revues sur le sujet "Endosomal TLRs"

Sato, Ryota, Tatjana Reuter, Ryosuke Hiranuma, et al. "The impact of cell maturation and tissue microenvironments on the expression of endosomal Toll-like receptors in monocytes and macrophages." International Immunology 32, no. 12 (2020): 785–98. http://dx.doi.org/10.1093/intimm/dxaa055.

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Abstract Toll-like receptors (TLRs) impact myeloid cell responsiveness to environmental cues such as pathogen components and metabolites. Although TLR protein expression in monocytes and tissue macrophages is thought to be optimized for microenvironments in each tissue, a comprehensive study has not been reported. We here examined protein expression of endogenous TLRs in tissue-resident myeloid cells. Neutrophils in peripheral blood, spleen, liver and lung expressed TLR2, TLR4 and TLR5 in all tissues. Ly6C+ MHC II‒ classical monocytes mature into Ly6C‒ MHC II+ monocyte-derived dendritic cells

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Luchner, Marina, Sören Reinke, and Anita Milicic. "TLR Agonists as Vaccine Adjuvants Targeting Cancer and Infectious Diseases." Pharmaceutics 13, no. 2 (2021): 142. http://dx.doi.org/10.3390/pharmaceutics13020142.

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Modern vaccines have largely shifted from using whole, killed or attenuated pathogens to being based on subunit components. Since this diminishes immunogenicity, vaccine adjuvants that enhance the immune response to purified antigens are critically needed. Further advantages of adjuvants include dose sparing, increased vaccine efficacy in immunocompromised individuals and the potential to protect against highly variable pathogens by broadening the immune response. Due to their ability to link the innate with the adaptive immune response, Toll-like receptor (TLR) agonists are highly promising a

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Patra, Mahesh Chandra, Asma Achek, Gi-Young Kim, et al. "A Novel Small-Molecule Inhibitor of Endosomal TLRs Reduces Inflammation and Alleviates Autoimmune Disease Symptoms in Murine Models." Cells 9, no. 7 (2020): 1648. http://dx.doi.org/10.3390/cells9071648.

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Toll-like receptors (TLRs) play a fundamental role in the inflammatory response against invading pathogens. However, the dysregulation of TLR-signaling pathways is implicated in several autoimmune/inflammatory diseases. Here, we show that a novel small molecule TLR-inhibitor (TAC5) and its derivatives TAC5-a, TAC5-c, TAC5-d, and TAC5-e predominantly antagonized poly(I:C) (TLR3)-, imiquimod (TLR7)-, TL8-506 (TLR8)-, and CpG-oligodeoxynucleotide (TLR9)-induced signaling pathways. TAC5 and TAC5-a significantly hindered the activation of nuclear factor kappa-light-chain-enhancer of activated B cel

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Hung, Yun-Fen, Chiung-Ya Chen, Yi-Chun Shih, Hsin-Yu Liu, Chiao-Ming Huang, and Yi-Ping Hsueh. "Endosomal TLR3, TLR7, and TLR8 control neuronal morphology through different transcriptional programs." Journal of Cell Biology 217, no. 8 (2018): 2727–42. http://dx.doi.org/10.1083/jcb.201712113.

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Neuroinflammation is associated with diverse neurological disorders. Endosomal Toll-like receptors (TLRs) including TLR3, TLR7, and TLR8 cell-autonomously regulate neuronal differentiation. However, the mechanisms by which these three TLRs affect neuronal morphology are unclear. In this study, we compare these TLRs in mouse neurons. By combining in vitro neuronal cultures, in utero electroporation, and transcriptomic profiling, we show that TLR8, TLR7, and TLR3 promote dendritic pruning via MYD88 signaling. However, they induce different transcriptomic profiles related to innate immunity, sign

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Veneziani, Irene, Claudia Alicata, Andrea Pelosi, et al. "Toll-like receptor 8 agonists improve NK-cell function primarily targeting CD56^brightCD16⁻ subset." Journal for ImmunoTherapy of Cancer 10, no. 1 (2022): e003385. http://dx.doi.org/10.1136/jitc-2021-003385.

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BackgroundToll-like receptors (TLRs) are pattern-recognition sensors mainly expressed in innate immune cells that directly recognize conserved pathogen structures (pathogen-associated molecular patterns-PAMPs). Natural killer (NK) cells have been described to express different endosomal TLRs triggered by RNA and DNA sequences derived from both viruses and bacteria. This study was addressed to establish which endosomal TLR could directly mediate NK activation and function after proper stimuli. It was also important to establish the most suitable TLR agonist to be used as adjuvant in tumor vacci

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Gallego, Carolina, Douglas Golenbock, Maria Adelaida Gomez, and Nancy Gore Saravia. "Toll-Like Receptors Participate in Macrophage Activation and Intracellular Control of Leishmania (Viannia) panamensis." Infection and Immunity 79, no. 7 (2011): 2871–79. http://dx.doi.org/10.1128/iai.01388-10.

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ABSTRACTToll-like receptors (TLRs) play a central role in macrophage activation and control of parasitic infections. Their contribution to the outcome ofLeishmaniainfection is just beginning to be deciphered. We examined the interaction ofLeishmania panamensiswith TLRs in the activation of host macrophages.L. panamensisinfection resulted in upregulation of TLR1, TLR2, TLR3, and TLR4 expression and induced tumor necrosis factor alpha (TNF-α) secretion by human primary macrophages at comparable levels and kinetics to those of specific TLR ligands. The TLR dependence of the host cell response was

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Mandraju, Rajakumar, Sean Murray, James Forman, and Chandrashekhar Pasare. "Differential regulation of CD8 T cell responses by surface and endosomal TLRs (INC6P.347)." Journal of Immunology 192, no. 1_Supplement (2014): 121.14. http://dx.doi.org/10.4049/jimmunol.192.supp.121.14.

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Abstract Sensing of pathogen/pathogen derived products through Toll like receptors (TLRs) induces dendritic cell (DC) maturation characterized by the expression of co-stimulatory molecules and secretion of pro-inflammatory cytokines. These two signals play a critical role in activation and differentiation of CD4 T cells. However, since the role of TLRs in the regulation of CD8 T cell responses is not clear we sought to address their role in this process. Our results show that although most TLRs induce the CD8 T cell proliferation in-vitro, there are significant differences in the CD8 T cell pr

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McAlpine, William, Lei Sun, Kuan-wen Wang, et al. "Excessive endosomal TLR signaling causes inflammatory disease in mice with defective SMCR8-WDR41-C9ORF72 complex function." Proceedings of the National Academy of Sciences 115, no. 49 (2018): E11523—E11531. http://dx.doi.org/10.1073/pnas.1814753115.

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The SMCR8-WDR41-C9ORF72 complex is a regulator of autophagy and lysosomal function. Autoimmunity and inflammatory disease have been ascribed to loss-of-function mutations of Smcr8 or C9orf72 in mice. In humans, autoimmunity has been reported to precede amyotrophic lateral sclerosis caused by mutations of C9ORF72. However, the cellular and molecular mechanisms underlying autoimmunity and inflammation caused by C9ORF72 or SMCR8 deficiencies remain unknown. Here, we show that splenomegaly, lymphadenopathy, and activated circulating T cells observed in Smcr8−/− mice were rescued by triple knockout

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Mauvieux, Laurent. "TLR1-10 Protein Expression in Circulating Human White Blood Cells during Bacterial and COVID-19 Infections." Blood 142, Supplement 1 (2023): 5349. http://dx.doi.org/10.1182/blood-2023-179266.

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Toll-like Receptors (TLR) are major sensors of the innate immune system and are involved in the recognition of Pathogen Associated Molecular Patterns (PAMPs) and Damage Associated Molecular Patterns (DAMPs). When activated, TLR signaling pathways trigger an intracellular response that leads to the production of pro-inflammatory cytokines, chemotactic factors, antimicrobial peptides, and interferons. Overexpression of certain TLRs on neutrophils has been associated with increased mortality in patients with infection-induced shock, although the role of TLR4 overexpression is still debated. While

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Ohto, Umeharu, Hiromi Tanji, Takuma Shibata, et al. "Structural studies of nucleic acid sensing Toll-like receptor." Acta Crystallographica Section A Foundations and Advances 70, a1 (2014): C252. http://dx.doi.org/10.1107/s2053273314097472.

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Toll-like receptors (TLRs) sense pathogen-associated molecular patterns originating from invading microorganism and evoke innate immune responses. Among TLRs, TLR3, TLR7, TLR8, and TLR9 are localized to endosomal membranes and are responsible for the recognition of nucleic acids. TLR7 and TLR8 recognize single stranded RNA. In addition, TLR7 and TLR8 are activated by small chemical compounds. TLR9 recognizes DNA containing Cytosine-phosphate-Guanine motif. Theses nucleic acid sensing TLRs are attractive therapeutic targets for the modulation of immune responses in the viral and bacterial infec

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Thèses sur le sujet "Endosomal TLRs"

CAPPELLETTI, CRISTINA. "Type I interferons and toll-like receptors are linked to pathological alterations of idiopathic inflammatory myopathiens." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2009. http://hdl.handle.net/10281/9235.

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Objective: The triggering factor of inflammation in idiopathic inflammatory myopathies (IIMs) is still unknown and an involvement of viruses or bacteria has been put forward. We sought to investigate the expression of type I interferons (IFNα/β) and of endosomal Toll-like receptors (TLRs) in IIM muscles. Methods: Ten IIM and 5 control muscle biopsies were assessed by microarray analysis for the expression of approximately 16,000 genes; 37 additional samples from IIM and controls were studied for IFNα/β-dependent genes and intracellular TLR expression using immunohistochemistry, confocal

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Combes, Alexis. "Caractérisation du rôle de BAD-LAMP comme chaperonne des "Toll like receptors" au sein des cellules dendritiques plasmacytoïdes humaines." Thesis, Aix-Marseille, 2016. http://www.theses.fr/2016AIXM4057.

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Les cellules dendritiques plasmacytoïdes humaines (pDCs) ont été montrées comme les principales cellules productrices d'interférons de type I (IFN) suivant une stimulation de leurs récepteurs TLRs intracellulaires. Après activation, les pDCs contrôlent la localisation subcellulaire de ces TLRs menant à une production séquentielle de cytokines. Une première vague d’IFN due la voie IRF dans les endosomes précoces, suivi de la production des cytokines pro-inflammatoires due à la voie NfκB dans les endosomes tardifs. BAD-LAMP/LAMP5, membre de la famille des protéines LAMP, spécifique du cerveau ch

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Actes de conférences sur le sujet "Endosomal TLRs"

Han, Xinbing, Xin Li, Medhavi Bole, et al. "Human Macrophages Recognize HIV SSRNA Through Endosomal TLR8." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a6252.

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Hasibuzzaman, MM, Briana Ibarra, Ishrat Khan, Caitlin D. Lemke-Miltner, George J. Weiner та Andrean L. Simons. "1125 In vitro characterization of cellular responses elicited by endosomal TLR agonists encapsulated in Qβ virus-like particles". У SITC 38th Annual Meeting (SITC 2023) Abstracts. BMJ Publishing Group Ltd, 2023. http://dx.doi.org/10.1136/jitc-2023-sitc2023.1125.

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