The PYRIN connection: Novel players in innate immunity and inflammation

被引:93
作者
Stehlik, C
Reed, JC
机构
[1] W Virginia Univ, Sch Med, Mary Babb Randolph Canc Ctr, Morgantown, WV 26506 USA
[2] W Virginia Univ, Sch Med, Dept Microbiol Immunol & Cell Biol, Morgantown, WV 26506 USA
[3] Burnham Inst, La Jolla, CA 92037 USA
关键词
D O I
10.1084/jem.20032234
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Periodic fever syndromes (PFSs) comprise a subset of the hereditary autoinflammatory disorders that are defined by recurrent self-resolving attacks of systemic inflammatory reactions in the absence of infection or autoimmunity. Recent advances have led to the discovery that members of a new family of genes, the PYRIN family, account for several hereditary PFSs. Here we discuss new insights into the function of PYRIN proteins and the molecular basis of PFSs.
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收藏
页码:551 / 558
页数:8
相关论文
共 44 条
[1]   A member of the Pyrin family, IFI16, is a novel BRCA1-associated protein involved in the p53-mediated apoptosis pathway [J].
Aglipay, JA ;
Lee, SW ;
Okada, S ;
Fujiuchi, N ;
Ohtsuka, T ;
Kwak, JC ;
Wang, Y ;
Johnstone, RW ;
Deng, CX ;
Qin, J ;
Ouchi, T .
ONCOGENE, 2003, 22 (55) :8931-8938
[2]   NALP3 forms an IL-lβ-Processing inflammasome with increased activity in Muckle-Wells autoinflammatory disorder [J].
Agostini, L ;
Martinon, F ;
Burns, K ;
McDermott, MF ;
Hawkins, PN ;
Tschopp, J .
IMMUNITY, 2004, 20 (03) :319-325
[3]   De novo CIAS1 mutations, cytokine activation, and evidence for genetic heterogeneity in patients with neonatal-onset multisystem inflammatory disease (NOMID) -: A new member of the expanding family of pyrin-associated autoinflammatory diseases [J].
Aksentijevich, I ;
Nowak, M ;
Mallah, M ;
Chae, JJ ;
Watford, WT ;
Hofmann, SR ;
Stein, L ;
Russo, R ;
Goldsmith, D ;
Dent, P ;
Rosenberg, HF ;
Austin, F ;
Remmers, EF ;
Balow, JE ;
Rosenzweig, S ;
Komarow, H ;
Shoham, NG ;
Wood, G ;
Jones, J ;
Mangra, N ;
Carrero, H ;
Adams, BS ;
Moore, TL ;
Schikler, K ;
Hoffman, H ;
Lovell, DJ ;
Lipnick, R ;
Barron, K ;
O'Shea, JJ ;
Kastner, DL ;
Goldbach-Mansky, R .
ARTHRITIS AND RHEUMATISM, 2002, 46 (12) :3340-3348
[4]   Cell activation and apoptosis by bacterial lipoproteins through toll-like receptor-2 [J].
Aliprantis, AO ;
Yang, RB ;
Mark, MR ;
Suggett, S ;
Devaux, B ;
Radolf, JD ;
Klimpel, GR ;
Godowski, P ;
Zychlinsky, A .
SCIENCE, 1999, 285 (5428) :736-739
[5]  
Bernot A, 1997, NAT GENET, V17, P25
[6]   Subcellular localisation of marenostrin/pyrin isoforms carrying the most common mutations involved in familial Mediterranean fever in the presence or absence of its binding partner ASC -: art. no. e24 [J].
Cazeneuve, C ;
Papin, S ;
Jéru, I ;
Duquesnoy, P ;
Amselem, S .
JOURNAL OF MEDICAL GENETICS, 2004, 41 (03)
[7]   The gene for familial Mediterranean fever, MEFV, is expressed in early leukocyte development and is regulated in response to inflammatory mediators [J].
Centola, M ;
Wood, G ;
Frucht, DM ;
Galon, J ;
Aringer, M ;
Farrell, C ;
Kingma, DW ;
Horwitz, ME ;
Mansfield, E ;
Holland, SM ;
O'Shea, JJ ;
Rosenberg, HF ;
Malech, HL ;
Kastner, DL .
BLOOD, 2000, 95 (10) :3223-3231
[8]   Targeted disruption of pyrin, the FMF protein, causes heightened sensitivity to endotoxin and a defect in macrophage apoptosis [J].
Chae, JJ ;
Komarow, HD ;
Cheng, J ;
Wood, G ;
Raben, N ;
Liu, PP ;
Kastner, DL .
MOLECULAR CELL, 2003, 11 (03) :591-604
[9]   Nods, Nalps and Naip: intracellular regulators of bacterial-induced inflammation [J].
Chamaillard, M ;
Girardin, SE ;
Viala, J ;
Philpott, DJ .
CELLULAR MICROBIOLOGY, 2003, 5 (09) :581-592
[10]   A novel enhancer of the Apaf1 apoptosome involved in cytochrome c-dependent caspase activation and apoptosis [J].
Chu, ZL ;
Pio, F ;
Xie, ZH ;
Welsh, K ;
Krajewska, M ;
Krajewski, S ;
Godzik, A ;
Reed, JC .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2001, 276 (12) :9239-9245