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Articles de revues sur le sujet « Endosomal TLRs »

Auteur : Grafiati

Publié le 9 mars 2023

Mis à jour le 31 juillet 2025

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1

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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Averett, D. R., S. P. Fletcher, W. Li, S. E. Webber, and J. R. Appleman. "The pharmacology of endosomal TLR agonists in viral disease." Biochemical Society Transactions 35, no. 6 (2007): 1468–72. http://dx.doi.org/10.1042/bst0351468.

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The discovery of endosomal TLRs (Toll-like receptors) and their natural ligands has accelerated efforts to exploit them for therapeutic benefit. Importantly, this was preceded by clinical exploration of agents now known to be endosomal TLR agonists. Clinical effects in viral disease have been reported with agonists of TLR3, TLR7, TLR7/8 and TLR9, and the TLR7 agonist imiquimod is marketed for topical use against warts, a papillomavirus disease. The observed pre-clinical and clinical profiles of agonists of each of these TLRs suggest induction of a multifaceted innate immune response, with biom

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Zahmatkesh, Azadeh, Elham Salmasi, and Reza Gholizadeh. "Interaction of toll-like receptors and ACE-2 with different variants of SARS-CoV-2: A computational analysis." BioImpacts 14, no. 4 (2024): 30150. http://dx.doi.org/10.34172/bi.2024.30150.

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Introduction: Computational studies were performed to investigate the unknown status of endosomal and cell surface receptors in SARS-CoV-2 infection. The interactions between Toll-like receptors (TLRs)- 4/7/8/9 or ACE2 receptor and different SARS-CoV-2 variants were investigated. Methods: The RNA motifs for TLR7, TLR8 and a CpG motif for TLR9 were analyzed in different variants. Molecular docking and molecular dynamics (MD) simulations were performed to investigate receptor-ligand interactions. Results: The number of motifs recognized by TLR7/8/9 in the Alpha, Delta and Iranian variants was lo

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Oleynik, Veronica A., Marina A. Plotnikova, Nikita D. Yolshin, Ekaterina A. Romanovskaya-Romanko, and Sergey A. Klotchenko. "Development and approbation of a quantitative PCR system for studying the expression of endosomal receptors and cytosolic nucleic acid sensors in mice." Medical academic journal 1, no. 1 (2025): 90–100. https://doi.org/10.17816/maj637237.

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BACKGROUND: The innate immune response plays a crucial role in protecting the organism against viral pathogens, important part of which are pattern recognition receptors, such as Toll-like and RIG-I-like receptors. It is known that viral invasion, including influenza virus infection, leads to the activation of intracellular pattern recognition receptors such as TLR3, TLR7, TLR8, and TLR9, which are localized in the endoplasmic reticulum, endosomes, and lysosomes, as well as MDA5 and RIG-I, which are cytosolic sensors of viral RNA not associated with cell membranes. The expression of these gene

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Carreto-Binaghi, Laura E., María Teresa Herrera, Silvia Guzmán-Beltrán, et al. "Reduced IL-8 Secretion by NOD-like and Toll-like Receptors in Blood Cells from COVID-19 Patients." Biomedicines 11, no. 4 (2023): 1078. http://dx.doi.org/10.3390/biomedicines11041078.

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Severe inflammatory responses are associated with the misbalance of innate and adaptive immunity. TLRs, NLRs, and cytokine receptors play an important role in pathogen sensing and intracellular control, which remains unclear in COVID-19. This study aimed to evaluate IL-8 production in blood cells from COVID-19 patients in a two-week follow-up evaluation. Blood samples were taken at admission (t1) and after 14 days of hospitalization (t2). The functionality of TLR2, TLR4, TLR7/8, TLR9, NOD1, and NOD2 innate receptors and IL-12 and IFN-γ cytokine receptors was evaluated by whole blood stimulatio

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von Hofsten, Susannah, Kristin Andreassen Fenton, and Hege Lynum Pedersen. "Human and Murine Toll-like Receptor-Driven Disease in Systemic Lupus Erythematosus." International Journal of Molecular Sciences 25, no. 10 (2024): 5351. http://dx.doi.org/10.3390/ijms25105351.

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The pathogenesis of systemic lupus erythematosus (SLE) is linked to the differential roles of toll-like receptors (TLRs), particularly TLR7, TLR8, and TLR9. TLR7 overexpression or gene duplication, as seen with the Y-linked autoimmune accelerator (Yaa) locus or TLR7 agonist imiquimod, correlates with increased SLE severity, and specific TLR7 polymorphisms and gain-of-function variants are associated with enhanced SLE susceptibility and severity. In addition, the X-chromosome location of TLR7 and its escape from X-chromosome inactivation provide a genetic basis for female predominance in SLE. T

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Lai, Chao-Yang, Yu-Wen Su, Kuo-I. Lin, Li-Chung Hsu, and Tsung-Hsien Chuang. "Natural Modulators of Endosomal Toll-Like Receptor-Mediated Psoriatic Skin Inflammation." Journal of Immunology Research 2017 (2017): 1–15. http://dx.doi.org/10.1155/2017/7807313.

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Psoriasis is a chronic inflammatory autoimmune disease that can be initiated by excessive activation of endosomal toll-like receptors (TLRs), particularly TLR7, TLR8, and TLR9. Therefore, inhibitors of endosomal TLR activation are being investigated for their ability to treat this disease. The currently approved biological drugs adalimumab, etanercept, infliximab, ustekinumab, ixekizumab, and secukizumab are antibodies against effector cytokines that participate in the initiation and development of psoriasis. Several immune modulatory oligonucleotides and small molecular weight compounds, incl

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Baumann, Christoph L., Irene M. Aspalter, Omar Sharif, et al. "CD14 is a coreceptor of Toll-like receptors 7 and 9." Journal of Experimental Medicine 207, no. 12 (2010): 2689–701. http://dx.doi.org/10.1084/jem.20101111.

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Recognition of pathogens by the innate immune system requires proteins that detect conserved molecular patterns. Nucleic acids are recognized by cytoplasmic sensors as well as by endosomal Toll-like receptors (TLRs). It has become evident that TLRs require additional proteins to be activated by their respective ligands. In this study, we show that CD14 (cluster of differentiation 14) constitutively interacts with the MyD88-dependent TLR7 and TLR9. CD14 was necessary for TLR7- and TLR9-dependent induction of proinflammatory cytokines in vitro and for TLR9-dependent innate immune responses in mi

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Mielcarska, Matylda Barbara, Magdalena Bossowska-Nowicka, Karolina Paulina Gregorczyk, Zbigniew Wyzewski, and Felix Ngosa Toka. "Tyrosine kinase Syk interacts with Hrs after TLR3 stimulation in murine microglial cells." Journal of Immunology 198, no. 1_Supplement (2017): 129.17. http://dx.doi.org/10.4049/jimmunol.198.supp.129.17.

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Abstract TLR3 (Toll-like receptor 3) belongs to the family of receptors involved in innate immune response. Present in endosomal compartment in cells, TLR3 recognizes the dsRNA (double-stranded RNA), viral nucleic acid or intermediate during viral replication and initiates signal transduction leading to inflammatory response. However, the first steps of signaling cascade occurring in cells immediately after TLR3 stimulation are still not well understood and require careful attention. In this paper we demonstrate that after poly(I:C) (dsRNA mimetic) stimulation of murine microglial cells (C8D1A

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Elshikha, Ahmed S., Georges Abboud, Rigena Avdiaj, Laurence Morel, and Sihong Song. "The Inhibitory Effects of Alpha 1 Antitrypsin on Endosomal TLR Signaling Pathways." Biomolecules 15, no. 1 (2025): 43. https://doi.org/10.3390/biom15010043.

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Endosomal toll-like receptors (TLRs) TLR7, TLR8, and TLR9 play an important role in systemic lupus erythematosus (SLE) pathogenesis. The proteolytic processing of these receptors in the endolysosome is required for signaling in response to DNA and single-stranded RNA, respectively. Targeting this proteolytic processing may represent a novel strategy to inhibit TLR-mediated pathogenesis. Human alpha 1 antitrypsin (hAAT) is a protease inhibitor with anti-inflammatory and immunoregulatory properties. However, the effect of hAAT on endosomal TLRs remains elusive. In this study, we first tested the

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Veneziani, Irene, Claudia Alicata, Lorenzo Moretta, and Enrico Maggi. "The Latest Approach of Immunotherapy with Endosomal TLR Agonists Improving NK Cell Function: An Overview." Biomedicines 11, no. 1 (2022): 64. http://dx.doi.org/10.3390/biomedicines11010064.

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Toll-like receptors (TLRs) are the most well-defined pattern recognition receptors (PRR) of several cell types recognizing pathogens and triggering innate immunity. TLRs are also expressed on tumor cells and tumor microenvironment (TME) cells, including natural killer (NK) cells. Cell surface TLRs primarily recognize extracellular ligands from bacteria and fungi, while endosomal TLRs recognize microbial DNA or RNA. TLR engagement activates intracellular pathways leading to the activation of transcription factors regulating gene expression of several inflammatory molecules. Endosomal TLR agonis

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Kalliolias, George D., Efthimia K. Basdra, and Athanasios G. Papavassiliou. "Targeting TLR Signaling Cascades in Systemic Lupus Erythematosus and Rheumatoid Arthritis: An Update." Biomedicines 12, no. 1 (2024): 138. http://dx.doi.org/10.3390/biomedicines12010138.

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Evidence from animal models and human genetics implicates Toll-like Receptors (TLRs) in the pathogenesis of Systemic Lupus Erythematosus (SLE) and Rheumatoid Arthritis (RA). Endosomal TLRs sensing nucleic acids were proposed to induce lupus-promoting signaling in dendritic cells, B cells, monocytes, and macrophages. Ligation of TLR4 in synovial macrophages and fibroblast-like synoviocytes (FLSs) by endogenous ligands was suggested to induce local production of mediators that amplify RA synovitis. Inhibition of TLRs using antagonists or monoclonal antibodies (mAbs) that selectively prevent extr

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Wang, Kuan-wen, Xiaoming Zhan, William McAlpine, et al. "Enhanced susceptibility to chemically induced colitis caused by excessive endosomal TLR signaling in LRBA-deficient mice." Proceedings of the National Academy of Sciences 116, no. 23 (2019): 11380–89. http://dx.doi.org/10.1073/pnas.1901407116.

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LPS-responsive beige-like anchor (LRBA) protein deficiency in humans causes immune dysregulation resulting in autoimmunity, inflammatory bowel disease (IBD), hypogammaglobulinemia, regulatory T (Treg) cell defects, and B cell functional defects, but the cellular and molecular mechanisms responsible are incompletely understood. In an ongoing forward genetic screen forN-ethyl-N-nitrosourea (ENU)-induced mutations that increase susceptibility to dextran sodium sulfate (DSS)-induced colitis in mice, we identified two nonsense mutations inLrba. Although Tregcells have been a main focus in LRBA rese

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Skert, Cristina, Manuela Fogli, Simone Perucca, et al. "Betaherpesvirus Reactivation and Toll-Like Receptor Expression After Allogeneic Stem Cell Transplantation." Blood 118, no. 21 (2011): 4924. http://dx.doi.org/10.1182/blood.v118.21.4924.4924.

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Abstract Abstract 4924 Introduction. β-herpesviruses, such as CMV and HHV6, are important pathogen in transplanted patients. The morbidity because of CMV reactivation after allogeneic stem cell transplantation (SCT) has led to the monitoring of this virus and to introduction of preemptive therapy. However, CMV infection is still one of the most challenging complications, because CMV disease may occur as life-threatening pneumonitis, and may increase the risk of opportunistic infections. HHV6 reactivation has been demonstrated after SCT and this virus is recognized as important pathogen, either

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Nelson, Alexander J., and Yee Ling WU. "Toll-like receptor signaling directly modulates B cell antibody responses." Journal of Immunology 204, no. 1_Supplement (2020): 151.28. http://dx.doi.org/10.4049/jimmunol.204.supp.151.28.

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Abstract Toll-like receptor (TLR) signaling alone or in concert with other cellular or molecular signals helps shape responses by different cell types. Murine B lymphocytes express cell surface-bound TLRs 1, 2, 4, 6 and endosomal TLRs 3, 7, 9. This study aims to delineate the effects of these TLRs on B cell responses including proliferation, activation and antibody class-switch recombination (CSR). We stimulated mature, naïve B cells in vitro with individual TLR agonists alone or together with T cell help (via ligation of CD40) and the TH2 cytokine interleukin-4 (IL-4). We measured proliferati

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Wang, James Q., Bruce Beutler, Christopher C. Goodnow, and Keisuke Horikawa. "Inhibiting TLR9 and other UNC93B1-dependent TLRs paradoxically increases accumulation of MYD88L265P plasmablasts in vivo." Blood 128, no. 12 (2016): 1604–8. http://dx.doi.org/10.1182/blood-2016-03-708065.

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Key Points Inhibiting endosomal TLRs suppresses MYD88L265P B-cell proliferation in vitro. Inhibition of endosomal TLRs paradoxically enhances accumulation of MYD88L265P B cells as plasmablasts in vivo.

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Ganguly, Dipyaman, Georgios Chamilos, Roberto Lande, et al. "Self-RNA–antimicrobial peptide complexes activate human dendritic cells through TLR7 and TLR8." Journal of Experimental Medicine 206, no. 9 (2009): 1983–94. http://dx.doi.org/10.1084/jem.20090480.

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Dendritic cell (DC) responses to extracellular self-DNA and self-RNA are prevented by the endosomal seclusion of nucleic acid–recognizing Toll-like receptors (TLRs). In psoriasis, however, plasmacytoid DCs (pDCs) sense self-DNA that is transported to endosomal TLR9 upon forming a complex with the antimicrobial peptide LL37. Whether LL37 also interacts with extracellular self-RNA and how this may contribute to DC activation in psoriasis is not known. Here, we report that LL37 can bind self-RNA released by dying cells, protect it from extracellular degradation, and transport it into endosomal co

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Ao, Da, Xueliang Liu, Sen Jiang, et al. "The Signal Peptide and Chaperone UNC93B1 Both Influence TLR8 Ectodomain Intracellular Endosomal Localization." Vaccines 10, no. 1 (2021): 14. http://dx.doi.org/10.3390/vaccines10010014.

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Toll-like receptor 8 (TLR8) is a single-stranded RNA sensing receptor and is localized in the cellular compartments, where it encounters foreign or self-nucleic acids and activates innate and adaptive immune responses. However, the mechanism controlling intracellular localization TLR8 is not completely resolved. We previously revealed the intracellular localization of TLR8 ectodomain (ECD), and in this study, we investigated the mechanism of the intracellular localization. Here we found that TLR8 ECDs from different species as well as ECDs from different TLRs are all intracellularly localized,

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Minton, Kirsty. "Regulation of endosomal TLRs." Nature Reviews Immunology 19, no. 11 (2019): 660–61. http://dx.doi.org/10.1038/s41577-019-0229-1.

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Lai, Chao-Yang, Da-Wei Yeh, Chih-Hao Lu, et al. "Thiostrepton inhibits psoriasis-like inflammation induced by TLR7, TLR8, and TLR9." Journal of Immunology 196, no. 1_Supplement (2016): 124.41. http://dx.doi.org/10.4049/jimmunol.196.supp.124.41.

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Abstract Toll-like receptors 7, 8 and 9 (TLR7-9) comprise a subfamily of TLR. Activation of these TLRs has been linked to the pathogenesis of autoimmune diseases such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and psoriasis. Thus antagonists of these TLRs are being investigated for their therapeutic applications on these diseases. Bortezomib is a proteasome inhibitor known to suppress activation of these TLRs. This drug is approved for the treatment of multiple myeloma, and its inhibitory effects on autoimmune disorders such as psoriasis, RA, and SLE have also been inves

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Elshikha, Ahmed Samir, Georges Abboud, Laurence Morel, and Sihong Song. "Targeting proteolytic cleavage of Toll-Like receptors by alpha-1 antitrypsin inhibited dendritic cells activation and function." Journal of Immunology 208, no. 1_Supplement (2022): 60.20. http://dx.doi.org/10.4049/jimmunol.208.supp.60.20.

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Abstract Toll-like receptors (TLRs) on dendritic cells (DC) interact with self-antigens and play a critical role in systemic lupus erythematosus (SLE) pathogenesis. TLR3, TLR7/8, or TLR9 are endosomal receptors that require proteolytic processing in the endolysosome to initiate signaling in response to DNA, single-stranded RNA, and double-stranded RNA. Targeting this proteolytic processing may represent a novel strategy for inhibiting TLR mediated pathogenesis. Human alpha 1 antitrypsin (hAAT) is a protease inhibitor with anti-inflammatory and immunoregulatory properties. However, the effect o

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Meibers, Hannah, Margaret McDaniel, and Chandrashekhar Pasare. "Vps33B is a crucial regulator of Type I Interferon response downstream of the cGAS-STING pathway." Journal of Immunology 204, no. 1_Supplement (2020): 68.13. http://dx.doi.org/10.4049/jimmunol.204.supp.68.13.

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Abstract Vacuolar protein sorting-associated protein 33B (Vps33B) plays a critical role in the trafficking of endosomal contents to lysosomes in macrophages, particularly following Toll-like receptor (TLR) activation. Upon activation by microbial ligands, TLRs are internalized into endosomes, then trafficked to lysosomes for degradation. We have previously shown that endosomal to lysosomal trafficking, and subsequent degradation of TLR4, is mediated by Vps33B. Without this crucial degradation step, TLRs remain trapped within altered endosomes, leading to an enhanced inflammatory response. Sinc

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Russo, Carla, Ivan Cornella-Taracido, Luisa Galli-Stampino, et al. "Small molecule Toll-like receptor 7 agonists localize to the MHC class II loading compartment of human plasmacytoid dendritic cells." Blood 117, no. 21 (2011): 5683–91. http://dx.doi.org/10.1182/blood-2010-12-328138.

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Abstract TLR7 and TLR8 are intracellular sensors activated by single-stranded RNA species generated during viral infections. Various synthetic small molecules can also activate TLR7 or TLR8 or both through an unknown mechanism. Notably, direct interaction between small molecules and TLR7 or TLR8 has never been shown. To shed light on how small molecule agonists target TLRs, we labeled 2 imidazoquinolines, resiquimod and imiquimod, and one adenine-based compound, SM360320, with 2 different fluorophores [5(6) carboxytetramethylrhodamine and Alexa Fluor 488] and monitored their intracellular loca

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Nahid, M., Lia Benso, John Shin, Huseyin Mehmet, Alexandra Hicks, and Ravisankar Ramadas. "Macrophage tolerance to MyD88-dependent TLR agonists is mediated by LPS-/R848-induced miR-146a (IRM12P.649)." Journal of Immunology 194, no. 1_Supplement (2015): 133.8. http://dx.doi.org/10.4049/jimmunol.194.supp.133.8.

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Abstract Toll like receptors (TLRs) TLRs facilitate the recognition of pathogens by immune cells and the initiation of the immune response, leading to the production of proinflammatory mediators. Production of proinflammatory mediators by innate immune cells such as macrophages is tightly regulated to facilitate pathogen clearance while limiting adverse impact on host tissue. Exposure to TLR ligands induces a state of temporary refractoriness to a subsequent exposure of a TLR ligand, a phenomenon referred to as ‘tolerance’. This study sought to evaluate the mechanistic regulation of TLR4 and T

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Paradowska-Gorycka, Agnieszka, Anna Wajda, Barbara Stypińska, et al. "The TLRs and IFNs in patients with connective tissue diseases." Postępy Polskiej Medycyny i Farmacji 7 (May 27, 2020): 1–10. http://dx.doi.org/10.5604/01.3001.0014.1583.

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Autoimmune connective tissue diseases (ACTD) are characterized by spontaneous stimulation of the immune system and the production of autoantibodies. Some autoantibodies may create an immune complex with DNA and/or RNA and promote tissue inflammation. Immune complexes that contain nucleic acids can act as ligands for endosomal Toll-like receptors (TLR), which activation induces secretion of the type I and type III interferons. The present study aimed to determine whether TLRs and IFNs genes could be considered as potential ACTD biomarkers. IFN-A and IFN-G showed a relationship with a predisposi

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Pawar, Kamlesh, Megumi Shigematsu, Soroush Sharbati, and Yohei Kirino. "Infection-induced 5′-half molecules of tRNAHisGUG activate Toll-like receptor 7." PLOS Biology 18, no. 12 (2020): e3000982. http://dx.doi.org/10.1371/journal.pbio.3000982.

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Toll-like receptors (TLRs) play a crucial role in the innate immune response. Although endosomal TLR7 recognizes single-stranded RNAs, their endogenous RNA ligands have not been fully explored. Here, we report 5′-tRNA half molecules as abundant activators of TLR7. Mycobacterial infection and accompanying surface TLR activation up-regulate the expression of 5′-tRNA half molecules in human monocyte-derived macrophages (HMDMs). The abundant accumulation of 5′-tRNA halves also occur in HMDM-secreted extracellular vehicles (EVs); the abundance of EV-5′-tRNAHisGUG half molecules is >200-fold high

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Radovic-Moreno, Aleksandar F., Natalia Chernyak, Christopher C. Mader, et al. "Immunomodulatory spherical nucleic acids." Proceedings of the National Academy of Sciences 112, no. 13 (2015): 3892–97. http://dx.doi.org/10.1073/pnas.1502850112.

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Immunomodulatory nucleic acids have extraordinary promise for treating disease, yet clinical progress has been limited by a lack of tools to safely increase activity in patients. Immunomodulatory nucleic acids act by agonizing or antagonizing endosomal toll-like receptors (TLR3, TLR7/8, and TLR9), proteins involved in innate immune signaling. Immunomodulatory spherical nucleic acids (SNAs) that stimulate (immunostimulatory, IS-SNA) or regulate (immunoregulatory, IR-SNA) immunity by engaging TLRs have been designed, synthesized, and characterized. Compared with free oligonucleotides, IS-SNAs ex

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Leifer, Cynthia, James Brooks, Jody Cameron, and Gabriela Chiosis. "The Heat Shock Protein gp96 play a multifaceted role in regulating Toll-like receptor 9 (136.40)." Journal of Immunology 184, no. 1_Supplement (2010): 136.40. http://dx.doi.org/10.4049/jimmunol.184.supp.136.40.

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Abstract Inappropriate activation and failure to inactivate Toll-like receptors (TLRs) contribute to immune mediated pathology. Nucleic acid sensing TLRs, including TLR9, are tightly regulated to prevent self DNA and RNA recognition, which can contribute to autoimmune disease. The overall goal of our research is to determine the molecular mechanisms governing nucleic acid sensing TLRs using TLR9 as a model. Regulation of TLR9 includes control of intracellular trafficking by association with proteins such as the endoplasmic reticulum chaperone gp96. Obligate proteolytic cleavage of TLR9 to an 8

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Park, Se-Ra, Dong-Jae Kim, Seung-Hyun Han, et al. "Diverse Toll-Like Receptors Mediate Cytokine Production by Fusobacterium nucleatum and Aggregatibacter actinomycetemcomitans in Macrophages." Infection and Immunity 82, no. 5 (2014): 1914–20. http://dx.doi.org/10.1128/iai.01226-13.

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ABSTRACTToll-like receptors (TLRs) orchestrate a repertoire of immune responses in macrophages against various pathogens.Fusobacterium nucleatumandAggregatibacter actinomycetemcomitansare two important periodontal pathogens. In the present study, we investigated TLR signaling regulating cytokine production of macrophages in response toF. nucleatumandA. actinomycetemcomitans. TLR2 and TLR4 are redundant in the production of cytokines (interleukin-6 [IL-6] and tumor necrosis factor alpha [TNF-α]) inF. nucleatum- andA. actinomycetemcomitans-infected macrophages. The production of cytokines by mac

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Leavy, Olive. "AP3 links endosomal TLRs and antigen presentation." Nature Reviews Immunology 12, no. 6 (2012): 400. http://dx.doi.org/10.1038/nri3232.

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Kiefer, Kerstin, Nathaniel Green, Michael Oropallo, Michael Cancro, and Ann Marshak-Rothstein. "BCR/TLR7 coligation uniquely drives plasma cell differentiation of autoreactive B cells (171.34)." Journal of Immunology 188, no. 1_Supplement (2012): 171.34. http://dx.doi.org/10.4049/jimmunol.188.supp.171.34.

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Abstract Endosomal Toll-like receptors (TLRs) play an important role in the manifestation of systemic autoimmune diseases such as SLE. In vitro, DNA-/RNA-associated autoantigens have been reported to activate B cells, pDCs, and other APCs, through TLR9/TLR7-dependent pathways. However, in vivo, TLR9 appears to negatively regulate TLR7-dependent responses. Hence, TLR9-/- autoimmune prone mice develop more severe disease and increased autoantibody titers against RNA associated proteins, while TLR7-/- and TLR7/9-/- autoimmune-prone mice develop less severe disease. AM14 BCR side-directed transgen

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Lin, You-Sheng, Yung-Chi Chang, Ting-Yu Lai, Chih-Yuan Lee, Tsung-Hsien Chuang, and Li-Chung Hsu. "The role of novel E3 ubiquitin ligase in the regulation of TLR3 signaling pathway." Journal of Immunology 204, no. 1_Supplement (2020): 226.26. http://dx.doi.org/10.4049/jimmunol.204.supp.226.26.

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Abstract Toll-like receptors (TLRs) are critical players in the host’s defense against infection by recognizing pathogen-associated molecular patterns (PAMPs) derived from microbes, and subsequently induce inflammatory responses, which eventually eliminate pathogens and repair damage tissues. However, excessive inflammation is detrimental to the host, and has been associated with the pathogenesis of various inflammatory and autoimmune diseases. Ubiquitination is a crucial strategy to alter protein function, expression, or cellular localization at the post-translational level, and has been show

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Mukhopadhyay, Subhankar, Audrey Varin, Yunying Chen, Baoying Liu, Karl Tryggvason, and Siamon Gordon. "SR-A/MARCO–mediated ligand delivery enhances intracellular TLR and NLR function, but ligand scavenging from cell surface limits TLR4 response to pathogens." Blood 117, no. 4 (2011): 1319–28. http://dx.doi.org/10.1182/blood-2010-03-276733.

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Abstract Phagocytic and pathogen sensing receptors are responsible for particle uptake and inflammation. It is unclear how these receptors' systems influence each other's function to shape an innate response. The class-A scavenger receptors SR-A (scavenger receptor A) and MARCO (macrophage receptor with collagenous structure) are 2 well-characterized phagocytic receptors that are unable to initiate inflammatory responses by themselves, yet are implicated in the pathogenesis of various inflammatory disorders. However, the mechanism for such an apparent discrepancy is still unclear. We utilized

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Shehab, Marwa, Rana Jammaz, Noor Salloum, and Elias A. Rahal. "Endosomal Toll-Like Receptors (TLRs) mediate enhancement of IL-17A production triggered by Epstein-Barr virus (EBV) DNA in mice." Journal of Infection in Developing Countries 12, no. 02.1 (2018): 26S. http://dx.doi.org/10.3855/jidc.10074.

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Introduction: EBV has long-been associated with autoimmune disorders. We have previously demonstrated that EBV DNA increases the production of IL-17A in mice. This property may play a role in the association of EBV with autoimmune diseases. The objective of this study was to elucidate mechanisms through which EBV DNA modulates IL-17A levels in mice. Methodology: To study the potential role of endosomal receptors in detecting EBV DNA, chloroquine, an endosomal maturation inhibitor, was used to treat mouse peripheral blood mononuclear cells (PBMCs) in the presence or absence of EBV DNA. IL

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Lehnardt, Seija, Thomas Wallach, Vitka Gres, and Philipp Henneke. "Guardians of neuroimmunity – Toll-like receptors and their RNA ligands." Neuroforum 25, no. 3 (2019): 185–93. http://dx.doi.org/10.1515/nf-2018-0032.

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Abstract RNA-sensing Toll-like receptors (TLRs) are mostly associated with the recognition of viruses. However, over the last years it has become clear that the function and relevance of these receptors are far more complex. They are essential for the recognition of bacteria, fungi and parasites, leading to transcriptional activation of central nervous system (CNS) resident and invading myeloid cells during infectious meningitis and encephalitis. Moreover, host-derived RNA species interact with TLRs. Injured CNS neurons release small RNAs, e. g. microRNAs, into the extracellular space. Neighbo

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Dela Justina, Vanessa, Fernanda R. Giachini, Fernanda Priviero, and R. Clinton Webb. "Double-stranded RNA and Toll-like receptor activation: a novel mechanism for blood pressure regulation." Clinical Science 134, no. 2 (2020): 303–13. http://dx.doi.org/10.1042/cs20190913.

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Abstract Toll-like receptors (TLRs), such as TLR4 and 9, recognize pathogen-associated molecular pattern (PAMPs) and danger-associated molecular patterns (DAMPs) and are associated with increased blood pressure (BP). TLR3, residing in the endosomal compartment, is activated by viral double-stranded RNA (dsRNA) leading to activation of TIR receptor domain-containing adaptor inducing IFN-β (TRIF) dependent pathway. Besides foreign pathogens, the immune system responds to endogenous markers of cellular damage such as mitochondrial dsRNA (mtdsRNA). New evidence has shown a link between dsRNA and i

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Lentini, Germana, Agata Famà, Giuseppe Valerio De Gaetano, et al. "Role of Endosomal TLRs in Staphylococcus aureus Infection." Journal of Immunology 207, no. 5 (2021): 1448–55. http://dx.doi.org/10.4049/jimmunol.2100389.

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Mielcarska, Matylda Barbara, Justyna Struzik, and Felix Ngosa Toka. "Tlr3 interacts with ESCRT-I components Tsg101 and Hcrp1 in mouse astrocyte cell line." Journal of Immunology 206, no. 1_Supplement (2021): 15.02. http://dx.doi.org/10.4049/jimmunol.206.supp.15.02.

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Abstract It is established now that ESCRT (endosomal sorting complex required for transport) complexes participate in the trafficking of endosomal Toll-like receptors (TLRs), which are relevant in the regulation of the TLR-mediated immune response. TLR3 plays a vital role in the innate immune control of herpes simplex type 1 virus (HSV-1) infection in the brain, however, the process of TLR3 delivery to the ligand recognition site and fate as endosomal cargo including the receptor degradation await explication. Proximity ligation assays in TLR3 agonist, poly(I:C) stimulated or unstimulated muri

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Lu, Chih-Hao, Chao-Yang Lai, Da-Wei Yeh, et al. "Involvement of M1 Macrophage Polarization in Endosomal Toll-Like Receptors Activated Psoriatic Inflammation." Mediators of Inflammation 2018 (December 16, 2018): 1–14. http://dx.doi.org/10.1155/2018/3523642.

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Psoriasis is a chronic inflammatory skin disorder that affects ~2%–3% of the worldwide population. Inappropriate and excessive activation of endosomal Toll-like receptors 7, 8, and 9 (TLRs 7–9) at the psoriatic site has been shown to play a pathogenic role in the onset of psoriasis. Macrophage is a major inflammatory cell type that can be differentiated into phenotypes M1 and M2. M1 macrophages produce proinflammatory cytokines, and M2 macrophages produce anti-inflammatory cytokines. The balance between these two types of macrophages determines the progression of various inflammatory diseases;

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García-Martínez, Karla Yvonne, Jingyi Chen, and Cynthia A. Leifer. "A Role for Stimulator of Interferon Genes in Toll-Like Receptor 8 Signaling." Journal of Immunology 210, no. 1_Supplement (2023): 161.04. http://dx.doi.org/10.4049/jimmunol.210.supp.161.04.

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Abstract The innate immune system is equipped with multiple receptors to detect microbial nucleic acids and induce type I interferon (IFN) to restrict viral replication. When dysregulated these receptor pathways induce inflammation in response to host nucleic acids and promote development and persistence of autoimmune diseases like Systemic Lupus Erythematosus (SLE). IFN production is regulated by the Interferon Regulatory Factor (IRF) transcription factor family downstream of several innate immune receptors such as Toll-like receptors (TLRs) and Stimulator of Interferon Genes (STING). Both TL

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Dominguez, Donye, Natalia Chernyak, Monica guan, et al. "Robust antitumor effects of SNA-based T cell therapy." Journal of Immunology 202, no. 1_Supplement (2019): 134.7. http://dx.doi.org/10.4049/jimmunol.202.supp.134.7.

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Abstract The use of toll like receptor (TLR) agonists for immunotherapy remains under intense investigation. Activation of TLRs unleash the power of dendritic cells (DCs) to induce a robust antitumor CD8+ T cell response. However, the role of TLRs in CD8+ T cells has been largely overlooked. T cells do express endosomal TLR9, but it is not readily targetable in these non-phagocytic cells. Using the novel delivery platform of spherical nucleic acids (SNAs), we have devised a way to efficiently activate endosomal TLR9 by CpG, while simultaneously delivering tumor antigens to intracellular compar

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