Inhibitors of apoptosis (IAPs) regulate intestinal immunity and inflammatory bowel disease (IBD) inflammation

被引：98

作者：

Pedersen, Jannie ^{[1
]}

LaCasse, Eric C. ^{[2
]}

Seidelin, Jakob B. ^{[1
]}

Coskun, Mehmet ^{[1
]}

Nielsen, Ole H. ^{[1
]}

机构：

[1] Univ Copenhagen, Herlev Hosp, Dept Gastroenterol, Med Sect, DK-2730 Herlev, Denmark

[2] Childrens Hosp Eastern Ontario, Res Inst, Apoptosis Res Ctr, Ottawa, ON K1H 8L1, Canada

来源：

TRENDS IN MOLECULAR MEDICINE | 2014年 / 20卷 / 11期

关键词：

anti-apoptotic proteins; inflammation; inflammatory bowel disease; intestine; signaling pathways; ubiquitin ligases; NF-KAPPA-B; X-LINKED INHIBITOR; TNF-ALPHA; XIAP DEFICIENCY; CELLULAR INHIBITORS; BARRIER FUNCTION; INNATE IMMUNITY; MOLECULAR-BASIS; PROTEINS IAPS; MAIT CELLS;

D O I：

10.1016/j.molmed.2014.09.006

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The inhibitor of apoptosis (IAP) family members, notably clAP1, clAP2, and XIAP, are critical and universal regulators of tumor necrosis factor (TNF) mediated survival, inflammatory, and death signaling pathways. Furthermore, IAPs mediate the signaling of nucleotide-binding oligomerization domain (NOD)1/NOD2 and other intracellular NOD-like receptors in response to bacterial pathogens. These pathways are important to the pathogenesis and treatment of inflammatory bowel disease (IBD). Inactivating mutations in the X-chromosome-linked IAP (XIAP) gene causes an immunodeficiency syndrome, X-linked lymphoproliferative disease type 2 (XLP2), in which 20% of patients develop severe intestinal inflammation. In addition, 4% of males with early-onset IBD also have inactivating mutations in XIAP. Therefore, the IAPs play a greater role in gut homeostasis, immunity and IBD development than previously suspected, and may have therapeutic potential.

引用

页码：652 / 665

页数：14

共 122 条

[1] MECHANISMS OF DISEASE Inflammatory Bowel Disease [J].