Toll-like receptors (TLRs) are a class of proteins
Endosomal Toll-Like Receptors (TLRs) mediate enhancement of IL-17A production triggered by Epstein-Barr virus (EBV) DNA in mice.
EBV has long-been associated with autoimmune disorders. We have previously shown that EBV DNA increases the production of IL-17A in mice. These properties may play a role in EBV association with autoimmune diseases. The purpose of this study was to explain the mechanism of EBV DNA in which modulate the levels of IL-17A in mice.To study the potential role of endosomal receptors in the detection of EBV DNA, chloroquine, endosomal maturation inhibitors, used to treat mice peripheral blood mononuclear cells (PBMC) in the presence or absence of EBV DNA. IL-17A levels were then assessed by ELISA.
Furthermore, to determine whether TLR3, 7 or 9 play a role in this pathway, a specific inhibitor used for these TLRs in both the rat PBMC and in vivo in BALB / c mice were treated with viral DNA; the level of IL-17A-17A then equal assessed.IL enhanced production of rat PBMCs cultured with EBV DNA; Pre-incubation of PBMC with chloroquine significantly reduce production.
When the cells were cultured with EBV DNA and TLR3, 7 or 9 inhibitor, a significant reduction in levels of IL-17A is detected. The same reduction in the production of IL-17A-induced EBV DNA in mice was observed when the animals were treated with TLR inhibitors.Endosomal TLRs appear to be involved in recognizing EBV DNA and then trigger the production of IL-17A in mice. The EBV is targeting this receptor positive subjects with delayed investigation of autoimmunity may be useful to assess whether they play the same role in humans.
Endosomal Toll-Like Receptors (TLRs) mediate enhancement of IL-17A production triggered by Epstein-Barr virus (EBV) DNA in mice.
MPMBP down-regulates Toll-like receptor (TLR) 2 ligand-induced production of proinflammatory cytokines by inhibiting NF-kB but not AP-1 activation.
MPMBP is a non-nitrogen-containing bisphosphonates new (non-NBP), which has an anti-bone resorptive activity and side chain antioxidants. This study aimed to assess the effect of MPMBP on the production of proinflammatory cytokines and chemokines by macrophage-like cell line, J774.1, in the presence of Toll-like receptor (TLR) agonist.
J774.1 cells were pretreated with or without MPMBP for 5 minutes, then incubated with or without Pam3Cys-Ser- (Lys) 4 (Pam3CSK4, TLR2 agonist) or lipid A (TLR4 agonist) for 24 hours. MPMBP down-regulated TLR2 ligand-induced production of IL-6, MCP-1, MIP-1α and TNF-α, but not TLR4 ligand-induced production of proinflammatory cytokines, and cytotoxic to cells J774.1. Cu-CPT22, TLR2 antagonist, down-regulated Pam3CSK4-induced production of IL-6, MCP-1 and MIP-1α, but not TNF-α. MPMBP inhibiting the translocation of NF-kB p65, but not p50, RelB, or p52 and inhibits the activation of JNK, but not p38 MAPK or ERK, in cells stimulated with Pam3CSK4 J774.1. Additionally, MPMBP not down-regulate AP-1 activation in cells stimulated with Pam3CSK4 J774.1 or lipid A. Our findings suggest that MPMBP inhibits the production of proinflammatory cytokines in cell J774.1 by pressing the activation of NF-kB p65 in TLR2, but not TLR4, track.
blocking the right of pulses like receptor (TLR) activation during development of the disease have been reported to have an inhibitory effect on the pathogenesis of rheumatoid arthritis (RA). We tested whether TLR4 inhibitor TAK-242 has potential as a drug for arthritis arthritis.The therapeutic effect of TAK-242 was tested in vitro using human rheumatoid fibroblast-like synoviocyte (FLS) MH7A lines or primary human FLS and adjuvant-induced arthritis (AIA) rats model.
Description: TLR4 Antibody: Toll-like receptors (TLRs) are signaling molecules that recognize different microbial products during infection and serve as an important link between the innate and adaptive immune responses. These proteins act through adaptor molecules such as MyD88 and TIRAP to activate various kinases and transcription factors such as Protein Kinase C (PKC) alpha/beta and NF-κB. Studies with TLR4-deficient mice indicate that the main ligand for TLR is lipopolysaccharide. Consequently, these mice also showed increased susceptibility to Gram-negative sepsis.
Description: TLR4 Antibody: Toll-like receptors (TLRs) are signaling molecules that recognize different microbial products during infection and serve as an important link between the innate and adaptive immune responses. These proteins act through adaptor molecules such as MyD88 and TIRAP to activate various kinases and transcription factors such as Protein Kinase C (PKC) alpha/beta and NF-κB. Studies with TLR4-deficient mice indicate that the main ligand for TLR is lipopolysaccharide. Consequently, these mice also showed increased susceptibility to Gram-negative sepsis.
Description: TLR4 Antibody: Toll-like receptors (TLRs) are signaling molecules that recognize different microbial products during infection and serve as an important link between the innate and adaptive immune responses. These proteins act through adaptor molecules such as MyD88 and TIRAP to activate various kinases and transcription factors such as Protein Kinase C (PKC) alpha/beta and NF-κB. Studies with TLR4-deficient mice indicate that the main ligand for TLR is lipopolysaccharide. Consequently, these mice also showed increased susceptibility to Gram-negative sepsis.
Description: TLR4 Antibody: Toll-like receptors (TLRs) are signaling molecules that recognize different microbial products during infection and serve as an important link between the innate and adaptive immune responses. These proteins act through adaptor molecules such as MyD88 and TIRAP to activate various kinases and transcription factors such as Protein Kinase C (PKC) alpha/beta and NF-κB. Studies with TLR4-deficient mice indicate that the main ligand for TLR is lipopolysaccharide. Consequently, these mice also showed increased susceptibility to Gram-negative sepsis.
Description: A polyclonal antibody against TLR4. Recognizes TLR4 from Human, Mouse, Rat. This antibody is Unconjugated. Tested in the following application: ELISA, IHC;ELISA:1:2000-1:5000, IHC:1:25-1:100
Description: A polyclonal antibody against TLR4. Recognizes TLR4 from Human, Mouse, Rat. This antibody is Unconjugated. Tested in the following application: IHC, ELISA;IHC:1:200-500.ELISA:1/10000
Description: A polyclonal antibody against TLR4. Recognizes TLR4 from Human, Mouse. This antibody is Unconjugated. Tested in the following application: WB, IHC, ELISA;WB:1/500-1/2000.IHC:1/100-1/300.ELISA:1/40000
Description: A polyclonal antibody against TLR4. Recognizes TLR4 from Human. This antibody is Unconjugated. Tested in the following application: ELISA, IHC;ELISA:1:1000-1:5000, IHC:1:50-1:200
Description: A polyclonal antibody against TLR4. Recognizes TLR4 from Human. This antibody is Unconjugated. Tested in the following application: ELISA, IHC;ELISA:1:1000-1:5000, IHC:1:50-1:200
Description: A polyclonal antibody against TLR4. Recognizes TLR4 from Human, Mouse, Rat, Bovin. This antibody is Unconjugated. Tested in the following application: ELISA, WB
Description: A polyclonal antibody against TLR4. Recognizes TLR4 from Human, Mouse, Rat. This antibody is Unconjugated. Tested in the following application: ELISA, WB, IHC;ELISA:1:2000-1:5000, WB:1:500-1:2000, IHC:1:25-1:100
