TLR7

Toll-like receptor 7, also known as TLR7, is is_associated_with::protein that in humans is encoded by the TLR7 is_associated_with::gene. Orthologs are found in mammals and birds. It is a member of the is_associated_with::toll-like receptor (TLR) family.

Function
The TLR family plays an important role in pathogen recognition and activation of is_associated_with::innate immunity. TLRs are highly conserved from Drosophila to humans and share structural and functional similarities. They recognize is_associated_with::pathogen-associated molecular patterns (PAMPs) that are expressed on infectious agents, and mediate the production of is_associated_with::cytokines necessary for the development of effective immunity. The various TLRs exhibit different patterns of expression. This gene is predominantly expressed in is_associated_with::lung, is_associated_with::placenta, and is_associated_with::spleen, and lies in close proximity to another family member, is_associated_with::TLR8, on human chromosome X.

TLR7 recognises single-stranded is_associated_with::RNA in is_associated_with::endosomes, which is a common feature of viral is_associated_with::genomes which are internalised by is_associated_with::macrophages and is_associated_with::dendritic cells.

Clinical significance
is_associated_with::Imiquimod acts upon TLR7.

TLR7 has been shown to play a significant role in the pathogenesis of autoimmune disorders such as is_associated_with::Systemic Lupus Erythematosus (SLE) as well as in the regulation of antiviral immunity. Although not yet fully elucidated, using an unbiased genome-scale screen with short hairpin RNA (shRNA), it has been demonstrated that the receptor TREML4 acts as an essential positive regulator of TLR7 signalling. In TREML4 -/- mice macrophages that are hyporesponsive to TLR7 agonists, macrophages fail to produce type I interferons due to impaired phosphorylation of the transcription factor is_associated_with::STAT1 by the mitogen-activated protein kinase p38 and decreased recruitment of the adaptor MyD88 to TLR7. TREML4 deficiency reduced the production of inflammatory cytokines and autoantibodies in MRL/lpr mice, suggesting that TRL7 is a vital component of antiviral immunity and a predecessor factor in the pathogenesis of rheumatic diseases such as SLE.