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TLRs. TLRs are members of the type-1 transmembrane glycoprotein family which can bind extracellular ligands and act as a transducer to sponsor proinflammatory signaling through ectodomain leucine-rich repeated (LRR) sequences and cytoplasmic Toll/interleukin-1 receptor (TIR) domain .
There are numerous studies in the literature investigating the influence of TLRs genetic variation to TB susceptibility in humans (reviewed in ).
Moreover, p31-43 is able to bind TLRs on mast cells, thus leading to the secretion of proinflammatory cytokines and to the maturation of B lymphocytes .
Previous disease association studies revealed the effect of TLRs on the development of chronic inflammatory disease, injury, and cancer .
(a) Microorganisms in the intestine provide pathogen-associated molecular patterns (PAMPs) that serve as ligands for different Toll-like receptors (TLRs) on the luminal or basolateral surface of the intestinal epithelial cells (IECs).
On the basis of present observation, we found that alum adjuvanated phage lysate bacterin produce sufficient expression level of TLRs and cytokines which in turn suggest alum adjuvanated phage lysate bacterin in comparison to plain lysate produce sufficient immune-protection in form of Th1, Th2, cell mediated and humoral immune response.
By binding to RAGE or TLRs, HMGB1 stimulates ROS production and activation of NF-[kappa]B, which triggers inflammation and fibrosis in diabetic hearts.
However, available experimental data support the role of IAP in catalyzing the breakdown of monophosphates and detoxifying bacterial LPS, CpG DNA, and flagellin as well as extracellular nucleotides, such as UDP, resulting in lower TLRs activation and regulating inflammation and gut microbiota.
Previous studies have demonstrated that polysaccharides activate cellular responses through TLRs, such as TLR2 and TLR4.
Neutrophils detect pathogens via TLRs and directly attack them, for example, through phagocytosis.
The elevated levels of the TLRs during IR may cause the organ to become susceptible to early inflammatory attacks.
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