Relevant bibliographies by topics / TLR signaling

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'TLR signaling'

Author: Grafiati
Published: 4 June 2021
Last updated: 19 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'TLR signaling.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "TLR signaling"

1

Kawai, Taro, and Shizuo Akira. "TLR signaling." Seminars in Immunology 19, no. 1 (February 2007): 24–32. http://dx.doi.org/10.1016/j.smim.2006.12.004.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Kawai, T., and S. Akira. "TLR signaling." Cell Death & Differentiation 13, no. 5 (January 20, 2006): 816–25. http://dx.doi.org/10.1038/sj.cdd.4401850.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Takeda, Kiyoshi, and Shizuo Akira. "TLR signaling pathways." Seminars in Immunology 16, no. 1 (February 2004): 3–9. http://dx.doi.org/10.1016/j.smim.2003.10.003.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Brown, J., H. Wang, G. N. Hajishengallis, and M. Martin. "TLR-signaling Networks." Journal of Dental Research 90, no. 4 (October 12, 2010): 417–27. http://dx.doi.org/10.1177/0022034510381264.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

O'Neill, Luke A. J. "'Fine tuning' TLR signaling." Nature Immunology 9, no. 5 (May 2008): 459–61. http://dx.doi.org/10.1038/ni0508-459.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Gough, N. R. "Stages of TLR Signaling." Science Signaling 1, no. 21 (May 27, 2008): ec195-ec195. http://dx.doi.org/10.1126/stke.121ec195.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

TAMAKI, YASUNOBU, YUYA TAKAKUBO, TOMOYUKI HIRAYAMA, YRJÖ T. KONTTINEN, STUART B. GOODMAN, MITSUNORI YAMAKAWA, and MICHIAKI TAKAGI. "Expression of Toll-like Receptors and Their Signaling Pathways in Rheumatoid Synovitis." Journal of Rheumatology 38, no. 5 (February 15, 2011): 810–20. http://dx.doi.org/10.3899/jrheum.100732.

Full text
Abstract:
Objective.Toll-like receptors (TLR) recognizing endogenous and exogenous danger signals could play a role in rheumatoid arthritis (RA). Our aim was to describe the presence, localization, and extent of expression of TLR and their adapters.Methods.TLR 1, 2, 3, 4, 5, 6, and 9 receptors, and myeloid differentiation primary response protein 88, Toll/interleukin receptor (TIR) domain-containing adapter protein MyD88 adapter-like, and TIR domain-containing adapter-inducing interferon/TIR-containing adapter molecule-1 adapters were analyzed in RA (n = 10) and osteoarthritis (OA; n = 5) samples using real-time polymerase chain reaction (PCR). Their colocalization with cellular markers CD68, CD15, CD3, CD4, CD8, CD20, dendritic cell lysosomal-associated membrane protein (DC-LAMP), CD123, and 5B5 was analyzed in double immunofluorescence staining.Results.In RA, ß-actin standardized messenger RNA of TLR 2, 3, and 9 (p < 0.001) were particularly high. TLR 5 and 6 were also elevated (p < 0.05), but TLR 1 and 4 and adapters did not differ between RA and OA. In double-staining, TLR and adapters were strongly labeled in myeloid and plasmacytoid dendritic cells (DC), moderately in CD68+ type A lining cells/macrophages, and weakly to moderately in 5B5+ type B lining cells/fibroblasts. CD3+/CD4+ and CD3+/CD8+ T cells and CD20+ B cells in perivenular areas and in lymphoid follicles were moderately TLR- and weakly adapter-positive. In OA, TLR and adapters were weakly immunolabeled in vascular, lining, and inflammatory cells.Conclusion.RA synovium showed abundant expression of TLR. RA synovitis tissue seems to be responsive to TLR ligands. DC, type A cells/macrophages, and type B cells/fibroblasts are, in that order from highest to lowest, equipped with TLR, suggesting a hierarchical responsiveness. In RA, danger-associated molecular patterns to TLR interactions may particularly drive DC to autoinflammatory and autoimmune cascades/synovitis.
APA, Harvard, Vancouver, ISO, and other styles
8

Jeyaseelan, Samithamby. "How TLR signaling is regulated." Trends in Microbiology 10, no. 10 (October 2002): 448. http://dx.doi.org/10.1016/s0966-842x(02)02448-4.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

VanHook, Annalisa M. "TLR signaling mediates pathogen avoidance." Science Signaling 8, no. 393 (September 8, 2015): ec254-ec254. http://dx.doi.org/10.1126/scisignal.aad3632.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

van Duin, David, Ruslan Medzhitov, and Albert C. Shaw. "Triggering TLR signaling in vaccination." Trends in Immunology 27, no. 1 (January 2006): 49–55. http://dx.doi.org/10.1016/j.it.2005.11.005.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "TLR signaling"

1

Buchta, Claire Marie. "Mechanisms of TLR signaling and cooperation in B lymphocytes." Diss., University of Iowa, 2014. https://ir.uiowa.edu/etd/4584.

Full text
Abstract:
B lymphocytes play important roles in antibody production, cytokine production, and antigen presentation to T cells. Ligation of Toll-like receptors (TLRs) on B cells stimulates cellular activation and B cell effector functions. Synergistic activation of other receptors such as CD40 or the B cell receptor (BCR) with TLR ligation further enhances B cell activation and effector functions. The tumor necrosis factor receptor associated factor (TRAF) family of proteins act as cytoplasmic signaling adaptor molecules and moderate downstream signaling from both the tumor necrosis factor receptor (TNFR) superfamily of proteins, including CD40, and the IL-1R/TLR superfamily of proteins. To date, only TRAFs 3 and 6 have been shown to be involved in TLR signaling, with TRAF6 providing positive regulation and TRAF3 providing negative regulation of TLR signaling in B cells. Deficiency in another TRAF family member, TRAF5, has been implicated in the development of atherosclerosis, a disease developed in part due to TLR dysregulation. Here, we addressed the hypothesis that TRAF5 is a negative regulator of TLR signaling. We found that TRAF5 negatively regulated TLR-mediated cytokine and antibody production in B lymphocytes. The enhanced cytokine production seen in TLR-stimulated TRAF5 KO B cells was not attributable to altered cellular survival or proliferation, but instead more cytokine was produced on a per-cell basis, likely due to enhanced MAPK pathways after TLR ligation. Additionally, TRAF5 deficiency did not dramatically affect cytokine production in TLR-stimulated bone marrow-derived macrophages or dendritic cells, suggesting that TRAF5 plays a greater role in TLR signaling in lymphoid versus myeloid cells. TRAF5 associated with the TLR signaling proteins MyD88 and TAB2, and negatively regulated the association of TAB2 with its binding partner TRAF6. Furthermore, we manipulated B cell activation via ligation of various TLRs, CD40, and/or the BCR in order to activate the cells to effectively present antigen. Activated B cells pulsed with antigen served as an effective cellular vaccine and offered protection against both an infectious pathogen (Listeria monocytogenes) and a model of murine melanoma. We identified two candidate activation criteria for B cell vaccines (Bvacs): stimulation through the BCR and TLR7, and stimulation through CD40 and TLR4. Additionally, we found that high IL-6 production by the activated Bvac was essential for inducing optimal CD8+ T cell memory. These B cell activation protocols offer significant advantages over those currently being tested for clinical use. Understanding B cell activation through TLRs is a critical step in developing new therapies against cancer and infectious disease.
APA, Harvard, Vancouver, ISO, and other styles
2

Wan, Youzhong. "THE FUNCTION OF INTERLEUKIN-1 RECEPTOR ASSOCIATED KINASE 2 IN TOLL-LIKE RECEPTOR-MEDIATED SIGNALING." Case Western Reserve University School of Graduate Studies / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=case1278430683.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Kim, Tae Whan. "The role of kinase activity of IRAK₄ in Tlr/il-1r mediated signaling." Cleveland, Ohio : Case Western Reserve University, 2008. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=case1228500771.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Kim, Tae Whan. "THE ROLE OF KINASE ACTIVITY OF IRAK4 IN TLR/IL-1R-MEDIATED SIGNALING." Case Western Reserve University School of Graduate Studies / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=case1228500771.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Lai, Jen-Feng. "The essential role of macrophages and TLR signaling in the host response to Mycoplasma pneumoniae." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2009. https://www.mhsl.uab.edu/dt/2010r/lai.pdf.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Lampropoulou, Vasiliki [Verfasser], and Roland [Akademischer Betreuer] Lauster. "TLR/MyD88 signaling in B cells suppresses T cell-mediated CNS autoimmunity / Vasiliki Lampropoulou. Betreuer: Roland Lauster." Berlin : Universitätsbibliothek der Technischen Universität Berlin, 2012. http://d-nb.info/1021976601/34.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Huang, Xuesong. "The Study on Signal Mechanism of Protein Kinase C zeta-involved NF-κB Activation in LPS-stimulated TLR4 Signaling Pathways." University of Toledo Health Science Campus / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=mco1193663177.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Vaughan, Tamisha Y. "Novel Mechanisms Underlying the Inflammatory Effects of Leptin and Low Dose Endotoxin." Diss., Virginia Tech, 2010. http://hdl.handle.net/10919/28013.

Full text
Abstract:
Obesity over the last several has become a major health concern in our country as well as the world. Obesity is also one of the risk factors which lead to several inflammatory complications such as diabetes, artherosclerosis, etc. Two leading factors involved in the causes of inflammatory complications include leptin and low dose endotoxin lipopolysaccharide (LPS). However, the mechanism underlying the involvement of these two mediators is not clearly understood. The purpose of this study is to understand the mechanism underlying inflammatory complications caused by leptin and low dose endotoxin most recently coined metabolic endotoxemia. Interleukin-Receptor Associated Kinase 1 (IRAK-1) is an intracellular signaling component shown to activate NFκB which leads to the induction of proinflammatory mediators. Deletion of IRAK-1 in mice has beneficial effects in alleviating inflammatory complications and human variations in IRAK-1 gene are correlated with higher risks for inflammatory diseases. Therefore, we hypothesized that IRAK-1 is critically involved for the induction of proinflammatory mediators induced by leptin and low dose LPS. IL-6 mRNA levels were measured in THP-1 (human monocytic cells) and wild type and IRAK-deficient bone marrow derived macrophages (BMDM) challenged with different combinations of leptin and LPS. Data shows that leptin alone will not induce inflammatory mediators. However, increased induction of IL-6 was observed in a synergistic manner involving both LPS and leptin in an IRAK-1 dependent manner causing a robust inflammatory response. With regard to the effect of low dose LPS, we observed that human monocytic cells treated with low concentrations of LPS showed a mild yet sustained induction of proinflammatory cytokines, which is contrast to the robust and transient induction of cytokines by a high dose LPS. To further determine the molecular mechanisms, we measured several key signaling molecules that include IRAK-1, IKKepsilon, and C/EBPdelta. Our study revealed a novel mechanism that appears to be distinct from the traditional NFï «B pathway responsible for the effect of low dose LPS.
Ph. D.
APA, Harvard, Vancouver, ISO, and other styles
9

Campbell, Sara J. "Mechanisms of Moraxella catarrhalis Induced Immune Signaling in the Pulmonary Epithelium." University of Toledo Health Science Campus / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=mco1268141520.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Faria, Camila Cristina Quinello Gomes de. "Avaliação da resposta imune após estimulação de monócitos via Toll-Like Receptor 2 (TLR-2) em recém-nascidos a termo e pré-termo." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/5/5141/tde-04022014-105154/.

Full text
Abstract:
O sistema imune neonatal tem sido considerado funcionalmente imaturo e recentes estudos sugerem que a suscetibilidade do neonato às infecções pode ser devido a alterações funcionais de células apresentadoras de antígenos que podem levar a deficiências secundárias nas respostas adaptativas. A ativação das células apresentadoras de antígenos é desencadeada pela estimulação de receptores, como os Toll-like Receptors (TLRs) e alterações na ativação desses receptores podem levar a uma subsequente redução da ativação de proteínas da via de sinalização intracelular e consequente alterações dos níveis das citocinas pró- e anti-inflamatórias, contribuindo assim, para uma resposta imune ineficiente do neonato. O Toll-like receptor 2 (TLR-2) é um receptor essencial para o reconhecimento seletivo de vários antígenos bacterianos e virais, em especial, o peptideoglicano, que compreende cerca de 50% da parede celular de bactérias Grampositivas, como os estafilococos, que são agentes infecciosos que prevalecem nas Unidades de Terapia Intensiva Neonatal. O objetivo deste estudo foi avaliar a ativação e resposta de monócitos de sangue do cordão umbilical de recém-nascidos pré-termo saudáveis < 34 semanas de gestação (Grupo 1), recém-nascidos pré-termo : 34 e < 37 semanas de gestação (Grupo 2) e recém-nascidos a termo (Grupo 3) e de adultos saudáveis, como controles, após a estimulação de TLR-2 ex-vivo com Pam3CSK4. Após a estimulação dos monócitos, foram determinados os níveis de expressão dos marcadores de ativação celular, os níveis das citocinas pró- e anti-inflamatórias e a expressão de moléculas envolvidas na sinalização intracelular. A caracterização das populações leucocitárias, bem como a capacidade fagocítica de Staphylococcus aureus e geração de burst oxidativo por monócitos e neutrófilos foram analisados por Citometria de Fluxo. Os resultados demonstraram que as células dendríticas e monócitos de neonatos expressam TLR-2 em níveis semelhantes aos de adultos. A expressão adequada de TLR-2 sugere um reconhecimento antigênico eficiente que é refletido em uma ativação apropriada das moléculas da cascata de sinalização e uma potente produção de citocinas pró-inflamatórias, apesar da reduzida produção de IL-10. Fagócitos neonatais apresentaram capacidade fagocítica de S. aureus reduzida em relação aos adultos e geração do burst oxidativo semelhante entre os grupos, no entanto neonatos prétermo apresentaram produção de peróxido de hidrogênio deficiente, o que poderia contribuir com uma reduzida morte intracelular deste microrganismo. Em conclusão, o recém-nascido não apresenta uma imaturidade funcional, mas sim, um desequilíbrio em sua resposta imune inata, com uma aparente menor produção de fatores antiinflamatórios, o que pode levar a predisposição à sepse
The neonatal immune system has been considered functionally immature and recent studies suggest that susceptibility of the neonate to infections may be due to functional alterations in antigen-presenting cells that can prompt to secondary deficiencies in adaptive responses. The activation of antigen-presenting cells is triggered by stimulation of receptors such as Toll-like receptors (TLRs) and changes in the activation of these receptors may lead to a subsequent reduction in the activation of intracellular signaling pathway proteins and consequent changes in pro- and anti-inflammatory cytokine levels, thus contributing to an inefficient immune response of the neonate. Toll-like Receptor 2 (TLR-2) is an essential receptor for the selective recognition of several bacterial and viral antigens, in particular, peptidoglycan, which comprises about 50% of the Gram-positive bacteria cell wall, such as staphylococci, which are infectious agents that prevail in Neonatal Intensive Care Units. The aim of this study was to evaluate the activation and response of monocytes derived from umbilical cord blood of healthy preterm newborns <34 weeks of gestation (Group 1), preterm newborns :34 and <37 weeks of gestation (Group 2) and term newborns (Group 3) and from healthy adults, as controls, after ex-vivo TLR-2 stimulation with Pam3CSK4. After monocyte stimulation, it was determined the expression levels of cellular activation markers, pro- and anti-inflammatory cytokine levels and the expression of molecules involved in downstream intracellular signaling. The characterization of leukocyte populations, as well as the phagocytic ability of Staphylococcus aureus and generation of oxidative burst by monocytes and neutrophils were analyzed by flow cytometry. The results demonstrated that neonatal dendritic cells and monocytes express TLR- 2 at similar levels to those of adults. The proper expression of TLR-2 suggests an efficient antigen recognition which is reflected in an appropriate activation of downstream signaling molecules and potent production of pro-inflammatory cytokines, in spite of the reduced production of IL-10. Neonatal phagocytes showed reduced phagocytic capacity of S. aureus compared to adults and similar generation of oxidative burst between groups, however preterm neonates showed deficient production of hydrogen peroxide, which could contribute to a reduced intracellular killing of this microorganism. In conclusion, the newborn does not present a functional immaturity, but an imbalance in its innate immune response, with an apparent lower production of antiinflammatory factors, which can lead to a predisposition to sepsis
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "TLR signaling"

1

Groves, Tim C. Pre-TCR and TCRab signaling during T cell development. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1997.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

Cheng, Gordon W. Functions of CD45 in TCR signaling in CD4p+sCD8p+s double-positive thymocytes. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1999.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

Mariathasan, Sanjeev. TCR-mediated signaling in thymocyte selection. 2001.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

Krawczyk, Connie Michele. Genetic dissection of signaling pathways downstream of the TCR and CD28. 2002.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

Geri, Guillaume, and Jean-Paul Mira. Host–pathogen interactions in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0306.

Full text
Abstract:
Infection by a pathogenic micro-organism triggers a coordinated activation of both innate and adaptive immune responses. The innate immune response quickly triggers an antimicrobial response that will initiate development of a pathogen-specific, long-lasting adaptive immune response. Accurate recognition of microbial-associated molecular patterns by pattern-recognition receptors (PRRs) is the cornerstone of this immediate response. Most studied PRRs are Toll-like receptors (TLRs) and their kinase signalling cascades that activate nuclear transcription factors, and induce gene expression and cytokine production. Deficiencies or genetic variability in these different signalling pathways may lead to recurrent pyogenic infections and severe invasive diseases. After initial contact between the host and pathogen, numerous factors mediate the inflammatory response, as pro-inflammatory cytokines and chemokines. Apart from host genetic variability, pathogen diversity also influences the phenotypic features of various infectious diseases. Genomic analysis may assist in the development of targeted therapies or new therapeutic strategies based on both patient and microorganism genotype.
APA, Harvard, Vancouver, ISO, and other styles

Book chapters on the topic "TLR signaling"

1

Stasi, Alessandra, Rossana Franzin, Giuseppe Stefano Netti, Elena Ranieri, Loreto Gesualdo, Giovanni Stallone, and Giuseppe Castellano. "TLR-4 Signaling in Pericytes." In Stem Cell Biology and Regenerative Medicine, 165–87. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-62129-2_7.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Colegio, Oscar R., and Ruslan Medzhitov. "TLR Signaling and Tumour-Associated Macrophages." In Tumour-Associated Macrophages, 119–33. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4614-0662-4_9.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Neagu, Monica, and Carolina Constantin. "Signal Transduction in Immune Cells and Protein Kinases." In Advances in Experimental Medicine and Biology, 133–49. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-49844-3_5.

Full text
Abstract:
AbstractImmune response relies upon several intracellular signaling events. Among the protein kinases involved in these pathways, members of the protein kinase C (PKC) family are prominent molecules because they have the capacity to acutely and reversibly modulate effector protein functions, controlling both spatial distribution and dynamic properties of the signals. Different PKC isoforms are involved in distinct signaling pathways, with selective functions in a cell-specific manner.In innate system, Toll-like receptor signaling is the main molecular event triggering effector functions. Various isoforms of PKC can be common to different TLRs, while some of them are specific for a certain type of TLR. Protein kinases involvement in innate immune cells are presented within the chapter emphasizing their coordination in many aspects of immune cell function and, as important players in immune regulation.In adaptive immunity T-cell receptor and B-cell receptor signaling are the main intracellular pathways involved in seminal immune specific cellular events. Activation through TCR and BCR can have common intracellular pathways while others can be specific for the type of receptor involved or for the specific function triggered. Various PKC isoforms involvement in TCR and BCR Intracellular signaling will be presented as positive and negative regulators of the immune response events triggered in adaptive immunity.
APA, Harvard, Vancouver, ISO, and other styles
4

Li, Ji-Kun, Jesse J. Balic, Liang Yu, and Brendan Jenkins. "TLR Agonists as Adjuvants for Cancer Vaccines." In Regulation of Inflammatory Signaling in Health and Disease, 195–212. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-5987-2_9.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Kobayashi, Koichi S. "Shaping Intestinal Bacterial Community by TLR and NLR Signaling." In World Review of Nutrition and Dietetics, 32–42. Basel: S. KARGER AG, 2013. http://dx.doi.org/10.1159/000346493.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Salcedo, Suzana Pinto, and Lena Alexopoulou. "Investigating TLR Signaling Responses in Murine Dendritic Cells Upon Bacterial Infection." In Host-Bacteria Interactions, 209–25. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1261-2_12.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Chang, J. Judy, and Marcus Altfeld. "Role of Toll-Like Receptor (TLR) Signaling in HIV-1-Induced Adaptive Immune Activation." In Humanized Mice for HIV Research, 275–87. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1655-9_23.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Gonçalves, João, Helena Soares, Norman L. Eberhardt, Sarah C. R. Lummis, David R. Soto-Pantoja, David D. Roberts, Umadas Maitra, et al. "TLR5." In Encyclopedia of Signaling Molecules, 1875–81. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_639.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Gonçalves, João, Helena Soares, Norman L. Eberhardt, Sarah C. R. Lummis, David R. Soto-Pantoja, David D. Roberts, Umadas Maitra, et al. "Tlr4." In Encyclopedia of Signaling Molecules, 1866. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_101371.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Gonçalves, João, Helena Soares, Norman L. Eberhardt, Sarah C. R. Lummis, David R. Soto-Pantoja, David D. Roberts, Umadas Maitra, et al. "TLR9." In Encyclopedia of Signaling Molecules, 1882. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_101373.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "TLR signaling"

1

Cleaver, Jeffrey O., Dahui You, Jeffrey Duggan, and Scott E. Evans. "Lung Epithelial TLR Signaling Is Essential To Inducible Resistance To Pneumonia." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a3272.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Anandaiah, Asha M., Medhavi Bole, Xin Li, Xiuqin Zhou, Benjamin A. Nelson, Souvenir D. Tachado, Henry Koziel, and Naimish R. Patel. "Vitamin D Upregulates TLR Signaling In HIV-infected Macrophages Exposed To Mycobacterium Tuberculosis." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a3225.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Ballinger, Megan N., Michael W. Newstead, Xianying Zeng, Bethany B. Moore, and Theodore J. Standiford. "The TLR Signaling Inhibitor IRAK-M Potentiates Bleomycin-Induced Lung Injury And Fibrosis." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a5413.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Golovatch, Polina, Divya Mehra, Vincent Lemaitre, and Jeanine D'Armiento. "The Role Of TLR Signaling In The Development Of Emphysema In ApoE-deficient Mice." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a6779.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Dadashian, Eman L., Sarah Herman, and Adrian Wiestner. "Abstract 2686: Dual inhibition of BCR and TLR signaling has therapeutic potential in chronic lymphocytic leukemia." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-2686.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Haria, Dhwani, Helena Kiefel, Yuliya Katlinskaya, Sunit Jain, Thomas Weinmaier, Shoko Iwai, Todd DeSantis, Toshi Takeuchi, Karim Dabbagh, and Kareem Graham. "Abstract 1490: Novel microbiome-derived peptides activate the host innate immune system by regulation of TLR signaling." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-1490.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Shen, Ping, Michael Fuchs, Marie Reisener, Clemens Gwinner, Peihua Wu, Tobias Jung, Matthias Pumberger, Carsten Perka, and Max Löhning. "FRI0523 TLR-1/2 SIGNALING IMPAIRS MITOCHONDRIAL OXIDATIVE PHOSPHORYLATION IN CHONDROCYTES VIA THE INDUCTION OF NITRIC OXIDE." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.3661.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Haria, Dhwani, Helena Kiefel, Yuliya Katlinskaya, Sunit Jain, Thomas Weinmaier, Shoko Iwai, Todd DeSantis, Toshi Takeuchi, Karim Dabbagh, and Kareem Graham. "Abstract 1490: Novel microbiome-derived peptides activate the host innate immune system by regulation of TLR signaling." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-1490.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Unger, Benjamin L., Andrea N. Faris, Shyamala Ganesan, Adam T. Comstock, Marc B. Hershenson, and Umadevi Sajjan. "Rhinovirus Suppresses TLR-Dependent IL-8 Responses In Airway Epithelial Cells By Interfering With MyD-88-Dependent Signaling Pathway." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a6879.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Kuo, Hsu-Ping, Sidney Hsieh, and Betty Chang. "Abstract 2598: Synergistic effect of ibrutinib and inhibitors targeting TLR signaling in ABC subtype of diffuse large B-Cell lymphoma." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-2598.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "TLR signaling"

1

Yingling, Jonathan, and Kiao-Fan Wang. Breast Tumorigenesis: Interaction of Two Signaling Pathways -- TGR-Beta Versus Estrogen Receptor. Fort Belvoir, VA: Defense Technical Information Center, September 1995. http://dx.doi.org/10.21236/ada302267.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Moeller, B., and A. Langley. TLS Fallback Signaling Cipher Suite Value (SCSV) for Preventing Protocol Downgrade Attacks. RFC Editor, April 2015. http://dx.doi.org/10.17487/rfc7507.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'TLR signaling' for particular source types:
Journal articles Dissertations / Theses
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography