Results 101 to 110 of about 238,767 (310)

Differential Expression and Regulation of Toll-Like Receptors (TLR) in Human Leukocytes: Selective Expression of TLR3 in Dendritic Cells [PDF]

open access: bronze, 2000
Marta Muzio   +10 more
openalex   +1 more source

Reprogramming of Fatty Acid Metabolism via PPARα‐Orchestrated FADS2 in Keratinocytes Modulates Skin Inflammation in Psoriasis

open access: yesAdvanced Science, EarlyView.
This study identifies fatty acid desaturase 2 (FADS2) as a key regulator linking polyunsaturated fatty acid (PUFA) metabolism to psoriatic inflammation. FADS2 deficiency impairs docosahexaenoic acid (DHA) biosynthesis, enhances NF‐κB signaling, and promotes neutrophil‐driven skin inflammation. PPARα transcriptionally activates FADS2, and its activation
Jiangluyi Cai   +19 more
wiley   +1 more source

The implication of dendritic cells in lung diseases: Immunological role of toll-like receptor 4

open access: yesGenes and Diseases
The immune responses play a profound role in the progression of lung lesions in both infectious and non-infectious diseases. Dendritic cells, as the “frontline” immune cells responsible for antigen presentation, set up a bridge between innate and ...
Shurui Xuan   +5 more
doaj   +1 more source

Emodin Alleviates Sepsis‐Induced Multiorgan Damage by Inhibiting NETosis through Targeting Neutrophils BCL‐10

open access: yesAdvanced Science, EarlyView.
Emodin targets BCL‐10 to modulate the BCL‐10/MALT1 complex, thereby suppressing NF‐κB activation and significantly exerting multiorgan protective effects in sepsis. Abstract Sepsis is a life‐threatening condition caused by dysregulated host responses to infection, characterized by excessive inflammation and abnormal coagulation.
Xiaolong Xu   +16 more
wiley   +1 more source

Toll-like receptor 4 imparts ligand-specific recognition of bacterial lipopolysaccharide [PDF]

open access: bronze, 2000
Egil Lien   +12 more
openalex   +1 more source

The CXCL10‐CXCR3 Axis Induces Tumor‐Associated Neutrophils to Interfere with CTLs‐Mediated Antitumor Activity in EBV‐Associated Epithelial Cancers

open access: yesAdvanced Science, EarlyView.
Compared with EBV‐negative epithelial cancer cells, EBV‐associated epithelial cancer cells exhibit enhanced secretion of chemokines, including CXCL10 and CCL5, to attract neutrophils. Via the CXCL10‐CXCR3 axis‐mediated positive feedback loop, neutrophils within EBV‐associated epithelial cancer cells are induced to form abundant NETs, which facilitate ...
Dijun Ouyang   +24 more
wiley   +1 more source

The Lipopolysaccharide-activated Toll-like Receptor (TLR)-4 Induces Synthesis of the Closely Related Receptor TLR-2 in Adipocytes [PDF]

open access: hybrid, 2000
Ying Lin   +5 more
openalex   +1 more source

The Pathogenic Roles of Local Vitamin D Metabolism Defect in Valve Inflammation and Calcification

open access: yesAdvanced Science, EarlyView.
This study identifies the valvular interstitial cell populations responsible for valvular calcification induced by hyperphosphatemia and likely aging, uncovers local vitamin D metabolism defect‐induced inflammation as a critical pathogenic factor of calcific aortic valve disease, and highlights active vitamin D and ERK inhibitor as potential preventive
Ruichen Yang   +10 more
wiley   +1 more source

Bacterial Lipopolysaccharide Activates NF-κB through Toll-like Receptor 4 (TLR-4) in Cultured Human Dermal Endothelial Cells [PDF]

open access: hybrid, 2000
Emmanuelle Faure   +8 more
openalex   +1 more source

Extracellular LCN2 Binding to 24p3R in Astrocytes Impedes α‐Synuclein Endocytosis in Parkinson's Disease

open access: yesAdvanced Science, EarlyView.
24p3R is an astrocytic receptor for α‐Syn uptake. When LCN2 is secreted from astrocytes, it binds to its receptor 24p3R in astrocytes and this binding impedes the α‐Syn PFF binding to 24p3R. This in turn inhibits 24p3R‐mediated α‐Syn PFF uptake and reduces the clearance of extracellular α‐Syn by astrocytes, which contributes to α‐Syn spread and ...
Ying‐Ying Jiao   +14 more
wiley   +1 more source

Home - About - Disclaimer - Privacy