Trypanosoma cruzi infection beats the B-cell compartment favouring parasite establishment: can we strike first?

ACOSTA E,; ZUNIGA, EI; MONTES, CAROLINA L; MERINO, MC; BERMEJO, D; AMEZCUA, C; MOTRAN, CLAUDIA CRISTINA; GRUPPI, ADRIANA

SCANDINAVIAN JOURNAL OF IMMUNOLOGY

WILEY-BLACKWELL PUBLISHING, INC

Año: 2007 vol. 66 p. 137 - 142

0300-9475

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.