Trypanosoma cruzi infection beats the B-cell compartment favouring parasite establishment: can we strike first?
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.
Acosta Rodriguez
E V
EV
Department of Clinical Biochemistry, School of Chemical Science, National University of Córdoba, Córdoba, Argentina.
Zuniga
E I
EI
Montes
C L
CL
Merino
M C
MC
Bermejo
D A
DA
Amezcua Vesely
M C
MC
Motran
C C
CC
Gruppi
A
A
D000818:Animals; D016175:B-Lymphocyte Subsets / Q000276:immunology* / Q000469:parasitology / Q000473:pathology*; D002454:Cell Differentiation / Q000276:immunology; D014355:Chagas Disease / Q000276:immunology* / Q000469:parasitology* / Q000473:pathology; D006801:Humans; D014349:Trypanosoma cruzi / Q000254:growth & development* / Q000276:immunology*