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.

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.

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

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.

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

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.

The cholesterol-sensing nuclear receptor LXR regulates inflammatory responses by altering the lipid composition of cell membranes.

The stimulation of lipopolysaccharides induced nuclear localization of IRAK2 to facilitate nuclear export of a specific subset of inflammation-related messenger RNAs for translation in murine macrophages.

B-1 cell unresponsiveness to antigen-stimulation is overcome during infections when Toll-like receptor engagement removes negative regulators of B cell receptor signaling, thereby supporting B-1 cell differentiation to IgM-secreting plasmablasts.