Trypanosoma cruzi Infection Beats the B-cell Compartment Favouring Parasite Establishment: Can we Strike First?

ACOSTA RODRIGUEZ EV, ZUNIGA EI, MONTES CL, MERINO MC, BERMEJO DA, AMEZCUA VESELY MC, MOTRAN CC, GRUPPI A

WILEY-BLACKWELL PUBLISHING, INC

Año: 2007 p. 137 - 137

p class="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.