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Both HEK293 (human origin) and embryonic bovine lung cells transfected with bTLR5 responded to addition of H7 flagellin (show FliC Proteins). Responses were significantly reduced when mutations were introduced into the TLR5-binding regions of H7 flagellin (show FliC Proteins).
TLR 5, 7, and 9 expression patterns differed between HPV-positive and -negative oropharyngeal squamous cell carcinoma patients. In HPV-positive tumors the expression of TLR 5 and 7 correlated with tumor recurrence.
These results suggest that HMGB1 (show HMGB1 Proteins)-modulated TLR5 signaling is responsible for pain hypersensitivity.
data show that TLR-5 and TLR-9 (show TLR9 Proteins) are susceptible genes to lupus nephritis (LN) and that their expression is dysregulated in LN patients' kidneys, supporting a role of these mediators in the pathogenesis of LN.
These results indicate that in Chinese genetic variation of TLR5 may be not a determinant of susceptibility to hepatitis B virus-related diseases but may play a role in development of hepatitis B virus-related severe liver diseases.
Distinctive Recognition of Flagellin (show FliC Proteins) by Human and Mouse Toll-Like Receptor 5
This study independently confirms the association of TLR5 c.1174C>T with protection against death in melioidosis, identifies lower bacteremia, IL-10 (show IL10 Proteins) and TNF-alpha (show TNF Proteins) production in carriers of the variant with melioidosis.
Study demonstrated that toll-like receptor 5 expression and functional activity as measured by interleukin 6 (show IL6 Proteins) are modulated by hormones
findings suggest that TLR5 is functionally expressed in the SG and responds to its cognate ligand flagellin (show FliC Proteins)
Upregulation of TLR4 (show TLR4 Proteins), TLR5, and TLR9 (show TLR9 Proteins) suggests the involvement of bacteria or dysregulation of the immune response to commensal flora in small bowel mucosa in irritable bowel syndrome patients.
that TLR5 is involved in the pathogenesis and dissemination of esophageal adenocarcinoma through as-yet-uncharacterized mechanisms
data directly demonstrate that nasal epithelial GM-CSF contributes to TLR5-mediated modulation of airway DCs and a subsequent IgA response.
The activation of NLRC4 (show NLRC4 Proteins) by flagellin (show FliC Proteins) downregulated the flagellin (show FliC Proteins)-induced and TLR5-mediated immune responses against flagellin (show FliC Proteins).
TLR5 but not NLRC4 (show NLRC4 Proteins) is required for S. pneumoniae FliC (show FliC Proteins)-induced protection.
This resulted in Sp1 displacement from the promoter and binding of Sp3 to it, leading to p300 recruitment and histone acetylation, activating transcription. This is the first study addressing the mechanisms of physiological TLR5 expression in the intestine. Additionally, a novel insight is gained into Sp1/Sp3-mediated gene regulation that may apply to other genes
TLR5 mediates CD172a (show SIRPA Proteins)(+) intestinal lamina propria dendritic cell induction of Th17 cells.
TLR5 activation plays an important role in the induction of podocyte apoptosis
TLR5 gene knockout impairs some effects of weight-reduction in diet-induced obesity (DIO). The glucose intolerance in DIO TLR5(-/-) mice was more significant than that in DIO C57BL/6 mice.
The results suggest that caveolin-1 (show CAV1 Proteins)/TLR5 signaling plays a key role in age-associated innate immune responses and that FlaB (show FliC Proteins)-PspA (show SFTPA1 Proteins) stimulation of TLR5 may be a new strategy for a mucosal vaccine adjuvant against pneumococcal infection in the elderly.
This study identified variations in the promoter that resulted in changes in TLR5 gene expression.
TLR5 takes part in the airway mucosal defense systems as a unique endogenous potentiator of airway serous secretions.
The results indicated that TLR5 SNPs were associated with the transcript abundance of cytokines.
This gene encodes a member of the toll-like receptor (TLR) family, which plays a fundamental role in pathogen recognition and activation of innate immune responses. These receptors recognize distinct pathogen-associated molecular patterns that are expressed on infectious agents. The protein encoded by this gene recognizes bacterial flagellin, the principal component of bacterial flagella and a virulence factor. The activation of this receptor mobilizes the nuclear factor NF-kappaB, which in turn activates a host of inflammatory-related target genes. Mutations in this gene have been associated with both resistance and susceptibility to systemic lupus erythematosus, and susceptibility to Legionnaire disease.
toll-like receptor 5
, toll/interleukin-1 receptor-like protein 3