Inhibitor of apoptosis (IAP) proteins in regulation of inflammation and innate immunity
Publikation: Bidrag til tidsskrift › Review › Forskning › fagfællebedømt
Standard
Inhibitor of apoptosis (IAP) proteins in regulation of inflammation and innate immunity. / Damgaard, Rune B; Gyrd-Hansen, Mads.
I: Discovery Medicine, Bind 11, Nr. 58, 2011, s. 221-31.Publikation: Bidrag til tidsskrift › Review › Forskning › fagfællebedømt
Harvard
APA
Vancouver
Author
Bibtex
}
RIS
TY - JOUR
T1 - Inhibitor of apoptosis (IAP) proteins in regulation of inflammation and innate immunity
AU - Damgaard, Rune B
AU - Gyrd-Hansen, Mads
PY - 2011
Y1 - 2011
N2 - Inflammatory and innate immune signaling in response to recognition of pathogens is essential for immunity and host survival. However, deregulation may lead to detrimental pathologies including immunodeficiency, inflammatory diseases, and cancer. Inhibitor of apoptosis (IAP) proteins have emerged as important regulators of innate immune signaling downstream of pattern recognition receptors (PRRs) such as Toll-like receptor 4 (TLR4), the nucleotide-binding oligomerization domain 1 (NOD1) and NOD2 receptors, and the retinoic acid-inducible gene (RIG)-I receptor. Recent evidence suggests that cIAP1, cIAP2, and XIAP facilitate ubiquitin-dependent signaling activated by these PRRs and mediate activation of nuclear factor-kappa B (NF-kappaB) transcription factors as well as the MAP kinases p38 and JNK. Here, we review the current understanding of IAP-mediated PRR signaling and how IAP proteins might present as promising targets for anti-inflammatory therapies in PRR-dependent inflammatory diseases including Crohn's disease, Blau syndrome, and septic shock.
AB - Inflammatory and innate immune signaling in response to recognition of pathogens is essential for immunity and host survival. However, deregulation may lead to detrimental pathologies including immunodeficiency, inflammatory diseases, and cancer. Inhibitor of apoptosis (IAP) proteins have emerged as important regulators of innate immune signaling downstream of pattern recognition receptors (PRRs) such as Toll-like receptor 4 (TLR4), the nucleotide-binding oligomerization domain 1 (NOD1) and NOD2 receptors, and the retinoic acid-inducible gene (RIG)-I receptor. Recent evidence suggests that cIAP1, cIAP2, and XIAP facilitate ubiquitin-dependent signaling activated by these PRRs and mediate activation of nuclear factor-kappa B (NF-kappaB) transcription factors as well as the MAP kinases p38 and JNK. Here, we review the current understanding of IAP-mediated PRR signaling and how IAP proteins might present as promising targets for anti-inflammatory therapies in PRR-dependent inflammatory diseases including Crohn's disease, Blau syndrome, and septic shock.
KW - Animals
KW - Humans
KW - Immunity, Innate
KW - Inflammation
KW - Inhibitor of Apoptosis Proteins
KW - NF-kappa B
KW - Nod2 Signaling
KW - Signal Transduction
KW - Toll-Like Receptor 4
M3 - Review
C2 - 21447281
VL - 11
SP - 221
EP - 231
JO - Discovery medicine
JF - Discovery medicine
SN - 1539-6509
IS - 58
ER -
ID: 40289977