Trypanosoma cruzi infection beats the B-cell compartment favouring parasite establishment: can we strike first?
Scand J Immunol
; 66(2-3): 137-42, 2007.
Article
em En
| MEDLINE
| ID: mdl-17635791
ABSTRACT
Trypanosoma cruzi, the causative agent of Chagas' disease, may sabotage humoral response by affecting B cells at the different stages of its development. The present review highlights the contributions of our laboratory in understanding how T. cruzi hinders B-cell generation and B-cell expansion limiting host defence and favouring its chronic establishment. We discuss how homoeostatic mechanisms can be triggered to control exacerbated B-cell proliferation that favour T. cruzi infection by eliminating parasite-specific B cells. Specific targeting of evasion mechanisms displayed in T. cruzi infection, as in vivo Fas/FasL blockade or Gal-3 expression inhibition, allowed us to modulate B-cell responses enhancing the anti-parasite humoral immune response. A comprehensive understanding of the biology of the B cell in health and disease is strictly required to devise immunointervention strategies aimed at enhancing protective immune responses during infections.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Trypanosoma cruzi
/
Subpopulações de Linfócitos B
/
Doença de Chagas
Limite:
Animals
/
Humans
Idioma:
En
Revista:
Scand J Immunol
Ano de publicação:
2007
Tipo de documento:
Article
País de afiliação:
Argentina
País de publicação:
ENGLAND
/
ESCOCIA
/
GB
/
GREAT BRITAIN
/
INGLATERRA
/
REINO UNIDO
/
SCOTLAND
/
UK
/
UNITED KINGDOM