Myd88 Dependent Pathway
Mostrando 1-12 de 21 artigos, teses e dissertações.
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1. Vias de transdução de sinal do receptor tipo Toll 4 nas células pancreáticas e seus efeitos na secreção e produção de insulina / Toll-like receptor 4 signal transduction pathways in pancreatic cells and their effect on insulin secretion and production
INTRODUÇÃO: O receptor tipo Toll 4 (TLR4) pertencente a uma família de receptores do sistema imune inato, reconhece o padrão molecular de lipopolissacarídeos (LPS), expressos por bactérias Gram negativas. Sua cascata de sinalização, nas células apresentadoras de antígeno, ocorre por duas vias principais: MyD88-dependente, que resulta na ativação
IBICT - Instituto Brasileiro de Informação em Ciência e Tecnologia. Publicado em: 28/08/2012
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2. Regulação do CD95L por PGE2 e seu impacto na morte de linfócitos T. / CD95L downregulation by PGE2 and its impact on T lymphocyte death.
Antigen-presenting cells (APCs) control T-cell responses by multiple mechanisms, including the expression of co-stimulatory molecules and the production of cytokines and other mediators that control T-cell proliferation, survival and differentiation. In this present work, it was demonstrated that soluble factor(s) produced by Toll-like receptor (TLR)-activat
Publicado em: 2008
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3. Mal connects TLR2 to PI3Kinase activation and phagocyte polarization
The recognition of bacterial lipoproteins by toll-like receptor (TLR) 2 is pivotal for inflammation initiation and control in many bacterial infections. TLR2-dependent signalling is currently believed to essentially require both adaptor proteins MyD88 (myeloid differentiation primary response gene 88) and Mal/TIRAP (MyD88-adapter-like/TIR-domain-containing a
Nature Publishing Group.
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4. Myeloid Differentiation Antigen 88 Deficiency Impairs Pathogen Clearance but Does Not Alter Inflammation in Borrelia burgdorferi-Infected Mice
The spirochete Borrelia burgdorferi causes acute inflammation in mice that resolves with the development of pathogen-specific adaptive immunity. B. burgdorferi lipoproteins activate innate immune cells via Toll-like receptor 2 (TLR2), but TLR2-deficient mice are not resistant to B. burgdorferi-induced disease, suggesting the involvement of other TLRs or non-
American Society for Microbiology.
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5. IL-18 and IL-33 elicit Th2 cytokines from basophils via a MyD88- and p38α-dependent pathway
IL-4 and IL-13 are instrumental in the development and progression of allergy and atopic disease. Basophils represent a key source of these cytokines and produce IL-4 and IL-13 when stimulated with IL-18, a member of the IL-1 family of cytokines. Comparative analyses of the effects of caspase-1-dependent IL-1 family cytokines on basophil IL-4 and IL-13 produ
The Society for Leukocyte Biology.
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6. Mycoplasma genitalium-Derived Lipid-Associated Membrane Proteins Activate NF-κB through Toll-Like Receptors 1, 2, and 6 and CD14 in a MyD88-Dependent Pathway ▿
Mycoplasma genitalium is a leading pathogen of nongonoccocal chlamydia-negative urethritis, which has been implicated directly in numerous other genitourinary and extragenitourinary tract pathologies. The pathogenesis of infection is attributed in part to excessive immune responses. M. genitalium-derived lipid-associated membrane proteins (LAMPs) are a mixtu
American Society for Microbiology (ASM).
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7. Lipopolysaccharide-Induced Activation of β2-Integrin Function in Macrophages Requires Irak Kinase Activity, p38 Mitogen- Activated Protein Kinase, and the Rap1 GTPase
Lipopolysaccharide (LPS), a component of the outer membrane of gram-negative bacteria, is a potent activator of macrophages. Besides inducing many transcriptional pathways, LPS also elicits rapid morphological changes such as cell spreading. Here we have investigated the signaling pathway that controls macrophage β2-integrin-dependent spreading in response
American Society for Microbiology.
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8. Micrococci and Peptidoglycan Activate TLR2→MyD88→IRAK→TRAF→NIK→IKK→NF-κB Signal Transduction Pathway That Induces Transcription of Interleukin-8
This study was done to elucidate the signal transduction pathway of interleukin-8 (IL-8) induction by gram-positive bacteria. Bacteria (micrococci) and peptidoglycan (PGN) induced transcription of IL-8 in HEK293 cells expressing Toll-like receptor 2 (TLR2) and CD14 but not in those expressing TLR1 or TLR4. A mutation within the NF-κB site in the IL-8 promot
American Society for Microbiology.
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9. Natural killer cell and macrophage cooperation in MyD88-dependent innate responses to Plasmodium falciparum
IFN-γ secretion by natural killer (NK) cells is pivotal to several tumor and viral immune responses, during which NK and dendritic cells cooperation is required. We show here that macrophages are mandatory for NK cell IFN-γ secretion in response to erythrocytes infected with Plasmodium falciparum (Pf), a causative agent of human malaria. In addition, direc
National Academy of Sciences.
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10. Involvement of the Toll-Like Receptor 9 Signaling Pathway in the Induction of Innate Immunity by Baculovirus†
We have previously shown that mice inoculated intranasally with a wild-type baculovirus (Autographa californica nuclear polyhedrosis virus [AcNPV]) are protected from a lethal challenge by influenza virus. However, the precise mechanism of induction of this protective immune response by the AcNPV treatment remained unclear. Here we show that AcNPV activates
American Society for Microbiology.
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11. Double-Stranded DNA Activates Glomerular Endothelial Cells and Enhances Albumin Permeability via a Toll-Like Receptor-Independent Cytosolic DNA Recognition Pathway
Viral DNA induces potent antiviral immunity by activating dendritic cells; however, the mechanism governing viral DNA-mediated triggering or aggravation of glomerulonephritis is unknown. Glomerular endothelial cells (GEnCs) do not express toll-like receptor (TLR)9, the only DNA-specific TLR. We therefore hypothesized that DNA could activate GEnCs via the rec
American Society for Investigative Pathology.
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12. Cell surface expression of an endoplasmic reticulum resident heat shock protein gp96 triggers MyD88-dependent systemic autoimmune diseases
Heat shock proteins have been implicated as endogenous activators for dendritic cells (DCs). Without tissue distress or death, these intracellular molecules are inaccessible to surface receptor(s) on DCs, possibly to avoid uncontrolled DC activation and breakdown of immunologic tolerance. We herein addressed this hypothesis in transgenic mice by enforcing ce
National Academy of Sciences.