Results 11 to 20 of about 85,956 (299)

MyD88 and beyond: a perspective on MyD88-targeted therapeutic approach for modulation of host immunity [PDF]

open access: yesImmunologic Research, 2021
The continuous emergence of infectious pathogens along with antimicrobial resistance creates a need for an alternative approach to treat infectious diseases.
K. Saikh
semanticscholar   +3 more sources

Schisandrin B Attenuates Diabetic Cardiomyopathy by Targeting MyD88 and Inhibiting MyD88‐Dependent Inflammation

open access: yesAdvanced Science, 2022
Diabetes manifests as chronic inflammation and leads to the development diabetic cardiomyopathy (DCM). Targeting key proteins in inflammatory signaling may provide new therapy for DCM.
Wu Luo   +9 more
semanticscholar   +4 more sources

Unresponsiveness of MyD88-deficient mice to endotoxin. [PDF]

open access: yesImmunity, 1999
MyD88 is a general adaptor protein that plays an important role in the Toll/IL-1 receptor family signalings. Recently, Toll-like receptors 2 and 4 (TLR2 and TLR4) have been suggested to be the signaling receptors for lipopolysaccharide (LPS).
T. Kawai   +4 more
semanticscholar   +3 more sources

The Bug in MyD88 Dependency [PDF]

open access: yesImmunity, 2006
The contribution of MyD88 adaptor-mediated signaling in immune responses to fungi is largely unexplored. In this issue of Immunity, show that MyD88 is dispensable in several aspects of dendritic-cell trafficking and T cell differentiation in response to a respiratory fungus.
van Lier, René A. W., Lutter, René
openaire   +3 more sources

Osteocytes directly regulate osteolysis via MYD88 signaling in bacterial bone infection

open access: yesNature Communications, 2022
The impact of bone cell activation on bacterially-induced osteolysis remains elusive. Here, we show that matrix-embedded osteocytes stimulated with bacterial pathogen-associated molecular patterns (PAMPs) directly drive bone resorption through an MYD88 ...
T. Yoshimoto   +10 more
semanticscholar   +1 more source

Sox4 represses host innate immunity to facilitate pathogen infection by hijacking the TLR signaling networks

open access: yesVirulence, 2021
Toll-like receptors (TLRs) are essential for the protection of the host from pathogen infections by initiating the integration of contextual cues to regulate inflammation and immunity.
Jian Shang   +10 more
doaj   +1 more source

Role of MyD88 in adenovirus keratitis [PDF]

open access: yesImmunology & Cell Biology, 2016
Pattern recognition receptors (PRRs) are critical to the early detection and innate immune responses to pathogens. In particular, the toll‐like receptor (TLR) system and its associated adaptor proteins have essential roles in early host responses to infection.
Zhou, Xiaohong   +5 more
openaire   +4 more sources

LncRNA NEAT1 activates MyD88/NF-κB pathway in bronchopneumonia through targeting miR-155-5p

open access: yesAutoimmunity, 2021
Background Bronchopneumonia is a disease of the respiratory tract. It leads to other complications and endangers life and health. Long non-coding RNA (lncRNA) participates in the occurrence and development of bronchopneumonia.
Ling-jia Chen   +9 more
doaj   +1 more source

Insights on the role of TLR-4 in neuroinflammation: a hint on COVID-19 relationship

open access: yesArchives of Pharmaceutical Sciences Ain Shams University, 2023
Neuroinflammation plays a crucial role in cognitive decline and neurodegenerative diseases, such as Alzheimer's. Within the central nervous system, microglia express Toll-like receptor 4 (TLR-4) abundantly, which prompts the secretion of proinflammatory ...
Salma A. Elshafey   +3 more
doaj   +1 more source

Extracellular HSP90α Induces MyD88-IRAK Complex-Associated IKKα/β−NF-κB/IRF3 and JAK2/TYK2−STAT-3 Signaling in Macrophages for Tumor-Promoting M2-Polarization

open access: yesCells, 2022
M2-polarization and the tumoricidal to tumor-promoting transition are commonly observed with tumor-infiltrating macrophages after interplay with cancer cells or/and other stroma cells.
Chi-Shuan Fan   +6 more
semanticscholar   +1 more source

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