TY - JOUR
T1 - Chronic inflammation
T2 - importance of NOD2 and NALP3 in interleukin-1beta generation
AU - Ferrero-Miliani, L
AU - Nielsen, O H
AU - Andersen, P S
AU - Girardin, S E
PY - 2007/2
Y1 - 2007/2
N2 - Inflammation is part of the non-specific immune response that occurs in reaction to any type of bodily injury. In some disorders, the inflammatory process - which under normal conditions is self-limiting - becomes continuous and chronic inflammatory diseases might develop subsequently. Pattern recognition molecules (PRMs) represent a diverse collection of molecules responsible for sensing danger signals, and together with other immune components they are involved in the first line of defence. NALP3 and NOD2, which belong to a cytosolic subgroup of PRMs, dubbed Nod-like-receptors (NLRs), have been associated recently with inflammatory diseases, specifically Crohn's disease and Blau syndrome (NOD2) and familial cold autoinflammatory syndrome, Muckle-Wells syndrome and chronic infantile neurological cutaneous and articular syndrome (NALP3). The exact effects of the defective proteins are not fully understood, but activation of nuclear factor (NF)-kappaB, transcription, production and secretion of interleukin (IL)-1beta and activation of the inflammasome are some of the processes that might hold clues, and the present review will provide a thorough update in this area.
AB - Inflammation is part of the non-specific immune response that occurs in reaction to any type of bodily injury. In some disorders, the inflammatory process - which under normal conditions is self-limiting - becomes continuous and chronic inflammatory diseases might develop subsequently. Pattern recognition molecules (PRMs) represent a diverse collection of molecules responsible for sensing danger signals, and together with other immune components they are involved in the first line of defence. NALP3 and NOD2, which belong to a cytosolic subgroup of PRMs, dubbed Nod-like-receptors (NLRs), have been associated recently with inflammatory diseases, specifically Crohn's disease and Blau syndrome (NOD2) and familial cold autoinflammatory syndrome, Muckle-Wells syndrome and chronic infantile neurological cutaneous and articular syndrome (NALP3). The exact effects of the defective proteins are not fully understood, but activation of nuclear factor (NF)-kappaB, transcription, production and secretion of interleukin (IL)-1beta and activation of the inflammasome are some of the processes that might hold clues, and the present review will provide a thorough update in this area.
KW - Carrier Proteins/immunology
KW - Chronic Disease
KW - Crohn Disease/immunology
KW - Humans
KW - Inflammation/immunology
KW - Interleukin-1beta/biosynthesis
KW - NLR Family, Pyrin Domain-Containing 3 Protein
KW - Nod2 Signaling Adaptor Protein/immunology
KW - Signal Transduction/immunology
U2 - 10.1111/j.1365-2249.2006.03261.x
DO - 10.1111/j.1365-2249.2006.03261.x
M3 - Review
C2 - 17223962
SN - 0009-9104
VL - 147
SP - 227
EP - 235
JO - Clinical and Experimental Immunology
JF - Clinical and Experimental Immunology
IS - 2
ER -