The role of NLRs and TLRs in the activation of the inflammasome.
BACKGROUND
Interleukin-1 beta is one of the most important pro-inflammatory cytokines. In contrast to other cytokines, activation of IL-1 beta requires processing from an inactive precursor by the cysteine protease caspase-1. Caspase-1 forms a protein platform called the inflammasome, together with proteins of the nucleotide-binding oligomerization domain-like receptor (NLR) family.


OBJECTIVE
A review of literature investigating the stimulation of IL-1 beta production by microbial pathogens and their components.


CONCLUSIONS
To produce IL-1 beta, macrophages need a double stimulation with Toll like receptor (TLR) ligands that induce gene transcription, and NLR agonists (such as ATP or muramyl dipeptide (MDP)) that activate the inflammasome. Monocytes can release active IL-1 beta upon stimulation with TLR ligands alone. This probably represents an adaptation of each cell type to its environment.
Netea
Mihai G
MG
Radboud University Nijmegen Medical Center, Nijmegen Institute for Infection, Inflammation and Immunity (N4i), Department of Medicine, Geert Grooteplein 8, 6525 GA Nijmegen, Netherlands.
van de Veerdonk
Frank L
FL
Kullberg
Bart Jan
BJ
Van der Meer
Jos W M
JW
Joosten
Leo A B
LA
D000818:Animals; D006801:Humans; D007249:Inflammation / Q000503:physiopathology*; D053583:Interleukin-1beta / Q000096:biosynthesis; D011956:Receptors, Cell Surface / Q000502:physiology*; D051193:Toll-Like Receptors / Q000502:physiology*
D053583:Interleukin-1beta; D011956:Receptors, Cell Surface; D051193:Toll-Like Receptors