Inhibition of IL-6 for the treatment of inflammatory diseases

被引：168

作者：

Nishimoto, N ^{[1
]}

Kishimoto, T ^{[1
]}

机构：

[1] Osaka Univ, Grad Sch Frontier Biosci, Lab Immune Regulat, Suita, Osaka 5650871, Japan

来源：

CURRENT OPINION IN PHARMACOLOGY | 2004年 / 4卷 / 04期

关键词：

D O I：

10.1016/j.coph.2004.03.005

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

Interleukin-6 (IL-6) is a pleiotropic cytokine with various biological activities. Deregulated overproduction of IL-6 has been found to play pathological roles in chronic inflammatory diseases such as rheumatoid arthritis, Castleman's disease, juvenile idiopathic arthritis and Crohn's disease. Humanized anti-IL-6 receptor antibody has been developed as a therapeutic agent for these diseases, and therapeutic benefits have been revealed in clinical studies.

引用

页码：386 / 391

页数：6

共 45 条

[1] Interleukin 6 is required for the development of collagen-induced arthritis [J].

Alonzi, T ;

Fattori, E ;

Lazzaro, D ;

Costa, P ;

Probert, L ;

Kollias, G ;

De Benedetti, F ;

Poli, V ;

Ciliberto, G .

JOURNAL OF EXPERIMENTAL MEDICINE, 1998, 187 (04) :461-468

[2] Blockade of interleukin 6 trans signaling suppresses T-cell resistance against apoptosis in chronic intestinal inflammation:: Evidence in Crohn disease and experimental colitis in vivo [J].

Atreya, R ;

Mudter, J ;

Finotto, S ;

Müllberg, J ;

Jostock, T ;

Wirtz, S ;

Schütz, M ;

Bartsch, B ;

Holtmann, M ;

Becker, C ;

Strand, D ;

Czaja, J ;

Schlaak, JF ;

Lehr, HA ;

Autschbach, F ;

Schürmann, G ;

Nishimoto, N ;

Yoshizaki, K ;

Ito, H ;

Kishimoto, T ;

Galle, PR ;

Rose-John, S ;

Neurath, MF .

NATURE MEDICINE, 2000, 6 (05) :583-588

[3] A point mutation of Tyr-759 in interleukin 6 family cytokine receptor subunit gp130 causes autoimmune arthritis [J].

Atsumi, T ;

Ishihara, K ;

Kamimura, D ;

Ikushima, H ;

Ohtani, T ;

Hirota, S ;

Kobayashi, H ;

Park, SJ ;

Saeki, Y ;

Kitamura, Y ;

Hirano, T .

JOURNAL OF EXPERIMENTAL MEDICINE, 2002, 196 (07) :979-990

[4] ALLEVIATION OF SYSTEMIC MANIFESTATIONS OF CASTLEMANS DISEASE BY MONOCLONAL ANTI-INTERLEUKIN-6 ANTIBODY [J].

BECK, JT ;

HSU, SM ;

WIJDENES, J ;

BATAILLE, R ;

KLEIN, B ;

VESOLE, D ;

HAYDEN, K ;

JAGANNATH, S ;

BARLOGIE, B .

NEW ENGLAND JOURNAL OF MEDICINE, 1994, 330 (09) :602-605

[5] Therapeutic benefit of blocking interleukin-6 activity with an anti-interleukin-6 receptor monoclonal antibody in rheumatoid arthritis - A randomized, double-blind, placebo-controlled, dose-escalation trial [J].

Choy, EHS ;

Isenberg, DA ;

Garrood, T ;

Farrow, S ;

Ioannou, Y ;

Bird, H ;

Cheung, N ;

Williams, B ;

Hazleman, B ;

Price, R ;

Yoshizaki, K ;

Nishimoto, N ;

Kishimoto, T ;

Panayi, GS .

ARTHRITIS AND RHEUMATISM, 2002, 46 (12) :3143-3150

[6] ANGIOGENESIS AND RHEUMATOID-ARTHRITIS - PATHOGENIC AND THERAPEUTIC IMPLICATIONS [J].

COLVILLENASH, PR ;

SCOTT, DL .

ANNALS OF THE RHEUMATIC DISEASES, 1992, 51 (07) :919-925

[7]

De Benedetti F, 1998, J RHEUMATOL, V25, P203

[8] ANGIOGENESIS IN CANCER, VASCULAR, RHEUMATOID AND OTHER DISEASE [J].

FOLKMAN, J .

NATURE MEDICINE, 1995, 1 (01) :27-31

[9] A SYSTEMIC LYMPHOPROLIFERATIVE DISORDER WITH MORPHOLOGIC FEATURES OF CASTLEMANS DISEASE - CLINICAL FINDINGS AND CLINICOPATHOLOGIC CORRELATIONS IN 15 PATIENTS [J].

FRIZZERA, G ;

PETERSON, BA ;

BAYRD, ED ;

GOLDMAN, A .

JOURNAL OF CLINICAL ONCOLOGY, 1985, 3 (09) :1202-1216

[10] EVIDENCE FOR CONTINUOUS STIMULATION OF INTERLEUKIN-6 PRODUCTION IN CROHNS-DISEASE [J].

GROSS, V ;

ANDUS, T ;

CAESAR, I ;

ROTH, M ;

SCHOLMERICH, J .

GASTROENTEROLOGY, 1992, 102 (02) :514-519

← 1 2 3 4 5 →