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What is the role of toll-like receptors in innate immune responses?

What is the role of toll-like receptors in innate immune responses?

Toll-like receptors (TLRs) are a class of pattern recognition receptors (PRRs) that initiate the innate immune response by sensing conserved molecular patterns for early immune recognition of a pathogen (1).

Which Toll-like receptor is activated specifically by viruses?

TLR mediate the antiviral immune responses by recognizing virus infection, activating signaling pathways and inducing the production of antiviral cytokines and chemokines. ssRNA and dsRNA viruses can be recognized by TLR7/8 and TLR3, respectively.

Are Toll-like receptors innate immunity?

The recent discovery and characterization of the Toll-like receptor (TLR) family have incited new interest in the field of innate immunity. It is already clear that these receptors have a vital role in microbial recognition, induction of antimicrobial genes and the control of adaptive immune responses.

How are toll-like receptors used in the innate immune system?

Toll-like Receptors in Antiviral Innate Immunity Toll-like receptors (TLRs) are fundamental sensor molecules of the host innate immune system, which detect conserved molecular signatures of a wide range of microbial pathogens and initiate innate immune responses via distinct signaling pathways.

What kind of receptors are toll like receptors?

Toll-like and C-Type Lectin Receptors Toll-like receptors (TLRs) are a family of at least 10 distinct transmembrane proteins that mediate the recognition of extracellular and endosomal microbial products.

How are TLRs involved in the development of innate immunity?

Recognition of microbial components by TLRs initiates signal transduction pathways, which triggers expression of genes. These gene products control innate immune responses and further instruct development of antigen-specific acquired immunity.

How are toll-like receptors used in diabetogenic T cells?

However, the preliminary results obtained using NOD mice bearing a non-functional TLR4 might suggest that TLR activation by self ligands is involved in the control of diabetogenic T cells. Maybe the “lesson” thought by exogenous TLR ligands is continuously reinforced via the activation of TLRs by endogenous ligands, like HSP60.