B- and T-cell responses in group a streptococcus M-protein- or Peptide-induced experimental carditis.
Infect Immun
; 77(5): 2177-83, 2009 May.
Article
em En
| MEDLINE
| ID: mdl-19273562
ABSTRACT
The etiology of rheumatic fever and rheumatic heart disease (RF/RHD) is believed to be autoimmune, involving immune responses initiated between streptococcal and host tissue proteins through a molecular mimicry mechanism(s). We sought to investigate the humoral and cellular responses elicited in a Lewis rat model of group A streptococcus M-protein- or peptide-induced experimental valvulitis/carditis, a recently developed animal model which may, in part, represent human rheumatic carditis. Recombinant streptococcal M5 protein elicited opsonic antibodies in Lewis rats, and anti-M5 antisera recognized epitopes within the B- and C-repeat regions of M5. One peptide from the streptococcal M5 protein B-repeat region (M5-B.6, amino acids 161 to 180) induced lymphocytes that responded to both recombinant M5 and cardiac myosin. Rats immunized with streptococcal M5 protein developed valvular lesions, distinguished by infiltration of CD3(+), CD4(+), and CD68(+) cells into valve tissue, consistent with human studies that suggest that RF/RHD are mediated by inflammatory CD4(+) T cells and CD68(+) macrophages. The current study provides additional information that supports the use of the rat autoimmune valvulitis model for investigating RF/RHD.
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Streptococcus pyogenes
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Proteínas da Membrana Bacteriana Externa
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Linfócitos B
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Linfócitos T
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Proteínas de Transporte
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Endocardite
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Anticorpos Antibacterianos
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Antígenos de Bactérias
Limite:
Animals
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Female
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Humans
Idioma:
En
Ano de publicação:
2009
Tipo de documento:
Article