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.
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 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.
Casein kinase 1G2 interacts with and inhibits the activation of receptor-interacting kinase 3, RIP3, in response to TNF and toll-like receptor family members and attenuates its necroptosis signaling activity.
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.