Structural brain plasticity is encoded in the topographic distribution of Toll receptors and their ability to switch between alternative signalling outcomes, thus translating diverse sensory experience into structural change.

The strength of Toll-like receptor signalling depends on the number and size of MyDDosomes formed as well as on how quickly these structures assemble.

A pattern recognition receptor called toll-like receptor 13 detects pathogens in a manner that is different to that seen in other pathogen sensors.

Microbial-sensing TLRs drive responses to the microbiota, while nucleic-acid sensing TLRs control responses to endogenous ligands, revealing novel regulation of B-1a responses through integrated BCR/TLR mediated activation.

The Toll-like receptor 2-4 genetic modification goat improves effectively resistance against Staphylococcus aureus infection by enhancing autophagy level, and it provides a novel strategy for challenge of S. aureus-caused infections.

In the context of susceptibility to severe COVID-19, the observations of a study provide the basis for a personalized interferon-based therapy in patients with rare TLR7 variants.

Sialoside-based pattern recognition by Siglecs directly regulates toll-like receptor signaling and a sialidase inhibitor protects against endotoxemia.

A pain-relaying ion channel on a hypersensitive population of sensory neurons can instead elicit sensations of itch in both fish and mice when directly activated, providing a novel model of itch transduction.

Determining that microbiota-deficient mice have increased visceral pain, which can be reversed by restoring microbiota, may lead to novel microbial-based strategies for disorders associated with visceral pain.

A transmembrane protein uses distinct mechanisms to regulate the movement of specific toll-like receptors-key immune system components involved in detecting pathogens-to their final locations inside cells.