Trypanosoma cruzi infection beats the B cell compartment favoring parasite establishment. Can we strike first?

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

SCANDINAVIAN JOURNAL OF IMMUNOLOGY

Año: 2007 p. 137 - 137

0300-9475

font face="AdvPSGAR3-I" size="2"> 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