Inflammatory heart disease: a role for cytokines

被引:77
作者
Fairweather, D
Rose, NR
机构
[1] Johns Hopkins Med Inst, W Harry Feinstone Dept Mol Microbiol & Immunol, Baltimore, MD 21205 USA
[2] Johns Hopkins Med Inst, Dept Pathol, Baltimore, MD 21205 USA
关键词
autoimmunity; cytokines; inflammation; myocarditis; virus;
D O I
10.1191/0961203305lu2192oa
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Inflammatory heart disease is a rising concern worldwide. Similar mechanisms link autoimmune diseases, including the association of increased disease with proinflammatory cytokines and the importance of regulatory mechanisms in the control of chronic inflammation. Many pathogens including bacteria, protozoa and viruses have been associated with heart disease in patients, and are able to induce similar disease in animal models. Recognition of pathogens by the innate immune system leads to release of proinflammatory cytokines that both reduce infection and increase chronic inflammatory heart disease. Elevated levels of proinflammatory cytokines are able to overcome tolerance to chronic disease, indicating that environmental factors are important in determining progression to chronic heart disease. Understanding the mechanisms leading to chronic heart disease will be critical for developing effective therapies to reduce cardiac dysfunction and heart failure.
引用
收藏
页码:646 / 651
页数:6
相关论文
共 30 条
[11]   IL-12 receptor β1 and Toll-like receptor 4 increase IL-1β- and IL-18-associated myocarditis and Coxsackievirus replication [J].
Fairweather, D ;
Yusung, S ;
Frisancho, S ;
Barrett, M ;
Gatewood, S ;
Steele, R ;
Rose, NR .
JOURNAL OF IMMUNOLOGY, 2003, 170 (09) :4731-4737
[12]   Myocarditis [J].
Feldman, AM ;
McNamara, D .
NEW ENGLAND JOURNAL OF MEDICINE, 2000, 343 (19) :1388-1398
[13]  
FONG IW, 2003, INFECT CARDIOVASCULA, P33
[14]   Mast cells in the development of adaptive immune responses [J].
Galli, SJ ;
Nakae, S ;
Tsai, M .
NATURE IMMUNOLOGY, 2005, 6 (02) :135-142
[15]  
GODENY EK, 1986, J IMMUNOL, V137, P1695
[16]  
Goodson NJ, 2004, HANDB SYST AUTOIMMUN, V1, P121
[17]   CARDIAC INJURY IN MYOCARDITIS INDUCED BY COXSACKIE-VIRUS GROUP-B, TYPE-3 IN BALB/C MICE IS MEDIATED BY LYT-2+ CYTOLYTIC LYMPHOCYTES [J].
GUTHRIE, M ;
LODGE, PA ;
HUBER, SA .
CELLULAR IMMUNOLOGY, 1984, 88 (02) :558-567
[18]   Vγ1+ T cells suppress and Vγ4+ T cells promote susceptibility to coxsackievirus B3-induced myocarditis in mice [J].
Huber, SA ;
Graveline, D ;
Newell, MK ;
Born, WK ;
O'Brien, RL .
JOURNAL OF IMMUNOLOGY, 2000, 165 (08) :4174-4181
[19]   An in vivo model of autoimmune post-coxsackievirus B3 myocarditis in severe combined immunodeficiency mouse [J].
Kishimoto, C ;
Hiraoka, Y ;
Takamatsu, N ;
Takada, H ;
Kamiya, H ;
Ochiai, H .
CARDIOVASCULAR RESEARCH, 2003, 60 (02) :397-403
[20]  
LANE JR, 1993, J IMMUNOL, V151, P1682