Modulatory effects on myocardial physiology induced by an anti-Trypanosoma cruzi monoclonal antibody involve recognition of major antigenic epitopes from beta1-adrenergic and M2-muscarinic cholinergic receptors without requiring receptor cross-linking.
J Neuroimmunol
; 153(1-2): 99-107, 2004 Aug.
Article
en En
| MEDLINE
| ID: mdl-15265668
ABSTRACT
It has been proposed that anti-myocardial antibodies (Ab) against neurotransmitter (NT) receptors are involved in the immunopathology of chronic Chagas' heart disease. We demonstrated that an anti-Trypanosoma cruzi monoclonal Ab (mAb), CAK20.12, binds to murine cardiac beta-adrenergic and muscarinic acetyl choline (mACh) receptors eliciting abnormal physiological responses on normal heart. No cross-linking requirement for mAb actions was demonstrated using Fab fragment derived from CAK20.12. mAb binding to synthetic peptides from the second extracellular loop of both beta1-adrenergic and mACh receptors, demonstrated by ELISA, identified the region of NT receptors involved. Cross-reactivity between these peptides and T. cruzi antigen was confirmed by binding inhibition assays. These results support the existence of cross-reactivity due to molecular mimicry between a parasite antigen and the major antigenic epitopes present on both beta1-adrenergic and M2-ACh receptors. Its possible relationship with cardiac dysfunction during chronic stage of Chagas' disease is also discussed.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Pindolol
/
Trypanosoma cruzi
/
Anticuerpos Antiprotozoarios
/
Receptores Adrenérgicos beta 1
/
Receptor Muscarínico M2
/
Anticuerpos Monoclonales
/
Contracción Miocárdica
Límite:
Animals
Idioma:
En
Revista:
J Neuroimmunol
Año:
2004
Tipo del documento:
Article
País de afiliación:
Argentina