Blocking IL-1 in systemic inflammation

被引：386

作者：

Dinarello, CA ^{[1
]}

机构：

[1] Univ Colorado, Div Infect Dis, Dept Med, Hlth Sci Ctr, Denver, CO 80262 USA

来源：

JOURNAL OF EXPERIMENTAL MEDICINE | 2005年 / 201卷 / 09期

关键词：

D O I：

10.1084/jem.20050640

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

A growing number of systemic inflammatory diseases characterized in part by recurrent fevers, leukocytosis, anemia, and elevated acute phase proteins are linked to interleukin (IL)-1 activity since rapid and sustained resolution is observed upon specific blockade of IL-1 receptors. Rapid resolution of systemic and local inflammation is now also reported in systemic onset juvenile idiopathic arthritis (SoJIA). Loss of control of the secretion of IL-1 beta might be a common mechanism explaining the aberrant activity of IL-1 in these diseases.

引用

页码：1355 / 1359

页数：5

共 27 条

[1] 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

[2] Phospholipases C and A2 control lysosome-mediated IL-1β secretion:: Implications for inflammatory processes [J].

Andrei, C ;

Margiocco, P ;

Poggi, A ;

Lotti, LV ;

Torrisi, MR ;

Rubartelli, A .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2004, 101 (26) :9745-9750

[3] The secretory route of the leaderless protein interleukin 1β involves exocytosis of endolysosome-related vesicles [J].

Andrei, C ;

Dazzi, C ;

Lotti, L ;

Torrisi, MR ;

Chimini, G ;

Rubartelli, A .

MOLECULAR BIOLOGY OF THE CELL, 1999, 10 (05) :1463-1475

[4] 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

[5] THE TYPE-II DECOY RECEPTOR - A NOVEL REGULATORY PATHWAY FOR INTERLEUKIN-1 [J].

COLOTTA, F ;

DOWER, SK ;

SIMS, JE ;

MANTOVANI, A .

IMMUNOLOGY TODAY, 1994, 15 (12) :562-566

[6]

Dailey NK, 2004, ARTHRITIS RHEUM, V50, pS440

[7] Anakinra for flares of pyogenic arthritis in PAPA syndrome [J].

Dierselhuis, MP ;

Frenkel, J ;

Wulffraat, NM ;

Boelens, JJ .

RHEUMATOLOGY, 2005, 44 (03) :406-408

[8] Infection, fever, and exogenous and endogenous pyrogens: some concepts have changed [J].

Dinarello, CA .

JOURNAL OF ENDOTOXIN RESEARCH, 2004, 10 (04) :201-222

[9] Biologic basis for interleukin-1 in disease [J].

Dinarello, CA .

BLOOD, 1996, 87 (06) :2095-2147

[10] Cytokine traps: multi-component, high-affinity blockers of cytokine action [J].

Economides, AN ;

Carpenter, LR ;

Rudge, JS ;

Wong, V ;

Koehler-Stec, EM ;

Hartnett, C ;

Pyles, EA ;

Xu, XB ;

Daly, TJ ;

Young, MR ;

Fandl, JP ;

Lee, F ;

Carver, S ;

McNnay, J ;

Bailey, K ;

Ramakanth, S ;

Hutabarat, R ;

Huang, TT ;

Radziejewski, C ;

Yancopoulos, GD ;

Stahl, N .

NATURE MEDICINE, 2003, 9 (01) :47-52

← 1 2 3 →