Next article Search Articles Instructions for authors  Access Statistics | Citation Manager  
MINI SYMPOSIUM: RHEUMATIC FEVER AND RHEUMATIC HEART DISEASE  

 Article Access Statistics
    Viewed7416    
    Printed333    
    Emailed2    
    PDF Downloaded966    
    Comments [Add]    
    Cited by others 7    

Recommend this journal

Genes, autoimmunity and pathogenesis of rheumatic heart disease


1 Heart Institute (InCor), School of Medicine, University of São Paulo, São Paulo;Institute for Immunology Investigation, National Institute for Science and Technology, University of São Paulo, São Paulo, Brazil
2 Heart Institute (InCor), School of Medicine, University of São Paulo, São Paulo;Institute for Immunology Investigation, National Institute for Science and Technology, University of São Paulo, São Paulo;Clinical Immunology and Allergy Division, School of Medicine, University of São Paulo, São Paulo, Brazil

Correspondence Address:
L Guilherme
Av. Dr. Eneas de Carvalho Aguiar, 44. 05403-903 São Paulo, SP
Brazil
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0974-2069.79617

Rights and Permissions

Year : 2011  |  Volume : 4  |  Issue : 1  |  Page : 13-21

 

SEARCH
Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles

  Article in PDF (542 KB)
Email article
Print Article
Add to My List
Pathogenesis of rheumatic heart disease (RHD) remains incompletely understood. Several genes associated with RHD have been described; most of these are involved with immune responses. Single nucleotide polymorphisms in a number of genes affect patients with RHD compared to controls. Molecular mimicry between streptococcal antigens and human proteins, including cardiac myosin epitopes, vimentin and other intracellular proteins is central to the pathogenesis of RHD. Autoreactive T cells migrate from the peripheral blood to the heart and proliferate in the valves in response to stimulation with specific cytokines. The types of cells involved in the inflammation as well as different cytokine profiles in these patients are being investigated. High TNF alpha, interferon gamma, and low IL4 are found in the rheumatic valve suggesting an imbalance between Th1 and Th2 cytokines and probably contributing to the progressive and permanent valve damage. Animal model of ARF in the Lewis rat may further contribute towards understanding the ARF.






[FULL TEXT] [PDF]*
 

 

 

 Next article
 Previous article
 Table of Contents

 Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
 
 
 Reader Comments
 Email Alert *
  *
 * Requires registration (Free)
 
 MINI SYMPOSIUM: RHEUMATIC FEVER AND RHEUMATIC HEART DISEASE
 




1 Heart Institute (InCor), School of Medicine, University of São Paulo, São Paulo;Institute for Immunology Investigation, National Institute for Science and Technology, University of São Paulo, São Paulo, Brazil
2 Heart Institute (InCor), School of Medicine, University of São Paulo, São Paulo;Institute for Immunology Investigation, National Institute for Science and Technology, University of São Paulo, São Paulo;Clinical Immunology and Allergy Division, School of Medicine, University of São Paulo, São Paulo, Brazil

Correspondence Address:
L Guilherme
Av. Dr. Eneas de Carvalho Aguiar, 44. 05403-903 São Paulo, SP
Brazil
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0974-2069.79617

Rights and Permissions

Pathogenesis of rheumatic heart disease (RHD) remains incompletely understood. Several genes associated with RHD have been described; most of these are involved with immune responses. Single nucleotide polymorphisms in a number of genes affect patients with RHD compared to controls. Molecular mimicry between streptococcal antigens and human proteins, including cardiac myosin epitopes, vimentin and other intracellular proteins is central to the pathogenesis of RHD. Autoreactive T cells migrate from the peripheral blood to the heart and proliferate in the valves in response to stimulation with specific cytokines. The types of cells involved in the inflammation as well as different cytokine profiles in these patients are being investigated. High TNF alpha, interferon gamma, and low IL4 are found in the rheumatic valve suggesting an imbalance between Th1 and Th2 cytokines and probably contributing to the progressive and permanent valve damage. Animal model of ARF in the Lewis rat may further contribute towards understanding the ARF.






[FULL TEXT] [PDF]*


        
Print this article     Email this article