Results 81 to 90 of about 151,127 (263)

АССОЦИАЦИЯ ПОЛИМОРФИЗМОВ ГЕНОВ TLR2, TLR4 И TLR6 С КОЛОНИЗАЦИЕЙ STREPTOCOCCUS PNEUMONIAE У РАБОТНИКОВ МЕТАЛЛУРГИЧЕСКОГО ПРОИЗВОДСТВА

open access: yesМедицина в Кузбассе
Работники предприятий черной металлургии подвергаются воздействию промышленных аэрозолей органической и неорганической природы, что может приводить к нарушению механизмов врожденного иммунитета и увеличению частоты респираторных инфекций.
Татьяна Викторовна Бушуева   +5 more
doaj   +1 more source

Deciphering and Targeting the Schwannoma‐Neuron‐Macrophage Crosstalk for the Treatment of Schwannomatosis and Associated Pain

open access: yesAdvanced Science, EarlyView.
We established patient‐derived SWN cell lines and orthotopic PDX models that recapitulate patient pain phenotypes, alongside a novel intravital DRG imaging platform to track macrophage infiltration and neuronal pain responses. Using these models, we define HMGB1–CCL2–IL‐6 signaling crosstalk driving pain and identify EGF signaling as a key regulator of
Zhenzhen Yin   +17 more
wiley   +1 more source

Activation of Ca2+-Dependent Signaling by TLR2 [PDF]

open access: yesThe Journal of Immunology, 2006
Abstract Upon contact with airway epithelial cells, bacterial products activate Ca2+ fluxes that are required for induction of NF-κB-dependent gene expression. TLR2 is apically displayed on airway cells, making it a likely transducer linking bacterial stimuli and kinases that affect Ca2+ release. Using biochemical and genetic approaches,
Jarin, Chun, Alice, Prince
openaire   +2 more sources

Analysis of TLR2 in Primary Endocrine Resistant of Breast Cancer

open access: yesFrontiers in Bioscience-Landmark
Background: Previous clinical studies have suggested that Toll-like receptor (TLR)2 had predictive function for endocrine resistance in HER2-positive breast cancer (BCa).
Yunmei Wang   +6 more
doaj   +1 more source

Contemporary views on inflammatory pain mechanisms: TRPing over innate and microglial pathways. [PDF]

open access: yes, 2016
Tissue injury, whether by trauma, surgical intervention, metabolic dysfunction, ischemia, or infection, evokes a complex cellular response (inflammation) that is associated with painful hyperalgesic states.
Guan, Zhonghui   +2 more
core   +2 more sources

A Functionally Conserved Enhancer is Critical for PGC1A Expression and Thermogenesis in Brown Fat

open access: yesAdvanced Science, EarlyView.
An evolutionarily conserved enhancer controls PGC1A expression and thermogenic activation in brown adipose tissue. Integrative multi‐omics analyses identify two BAT‐specific enhancers, with PGC1A‐En1 functioning as the dominant regulatory element that maintains thermogenic capacity across species.
Duo Su   +10 more
wiley   +1 more source

Leptin up-regulates TLR2 in human monocytes [PDF]

open access: yesJournal of Leukocyte Biology, 2013
Abstract Leptin-stimulated TLR2 and CD14 expression may potentiate innate immunity and inflammation, in obesity and T2DM. The adipokine leptin elicits changes in the expression of the activation markers CD40 and CD69 in PBMCs and DCs, yet its effect on PRRs remains to be elucidated. Serum leptin concentrations are elevated
Jaedicke KM   +5 more
openaire   +3 more sources

Gene silencing of Toll-like receptor 2 inhibits proliferation of human liver cancer cells and secretion of inflammatory cytokines. [PDF]

open access: yesPLoS ONE, 2012
BACKGROUND: Toll-like receptors (TLRs) are key factors in the innate immune system and initiate the inflammatory response to foreign pathogens such as bacteria, fungi and viruses.
Yuzheng Huang   +11 more
doaj   +1 more source

Cross-disease innate gene signature: Emerging diversity and abundance in RA comparing to SLE and SSc [PDF]

open access: yes, 2019
Overactivation of the innate immune system together with the impaired downstream pathway of type I interferon-responding genes is a hallmark of rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and systemic sclerosis (SSc).
Fillerová, Regina   +8 more
core   +1 more source

Hepatocyte BDNF Acts as a Novel Immune Checkpoint to Restrain TLR4‐Mediated Acute Hepatitis

open access: yesAdvanced Science, EarlyView.
This study identifies hepatocyte‐derived BDNF as an endogenous TLR4 antagonist that alleviates acute hepatitis. BDNF is downregulated in hepatocytes via REST‐mediated transcriptional repression during ALI/ALF. Mechanistically, BDNF binds to TLR4 on macrophages to suppress inflammation.
Weiwei Zhu   +15 more
wiley   +1 more source

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