Inhibitor of apoptosis (IAP) proteins in regulation of inflammation and innate immunity

Research output: Contribution to journalReviewResearchpeer-review

  • Rune B Damgaard
  • Mads Gyrd-Hansen
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.
Original languageEnglish
JournalDiscovery Medicine
Volume11
Issue number58
Pages (from-to)221-31
Number of pages11
ISSN1539-6509
Publication statusPublished - 2011

    Research areas

  • Animals, Humans, Immunity, Innate, Inflammation, Inhibitor of Apoptosis Proteins, NF-kappa B, Nod2 Signaling, Signal Transduction, Toll-Like Receptor 4

ID: 40289977