Human B cells infected by Trypanosoma cruzi undergo F-actin disruption and cell death via caspase-7 activation and cleavage of phospholipase Cgama1
Immunobiology, v. 225,n. 3, 151904, jan. 2020
Article
em En
| SES-SP, SESSP-IBPROD, SES-SP
| ID: bud-2906
Biblioteca responsável:
BR78.1
ABSTRACT
B cells contribute to the immune system in many ways such as antigen presentation to CD4+ T cells, secretion of cytokines and lymphoid tissue organogenesis. Furthermore, they are the only cell type capable of producing immunoglobulins. B cells also account for critical aspects of the resistance against intracellular pathogens. Trypanosoma cruzi is an intracellular parasite that sabotages humoral response by depletion of immature B cells. Polyclonal activation and secretion of non-specific antibodies are also other mechanisms used by T cruzi to evade and subvert the mammalian host immune system, leading to increased parasitemia and susceptibility to Chagas’ disease. It remained unclear whether B cell depletion occurs due to direct contact with T. cruzi or results from a global increase in inflammation. Unlike previous reports, we demonstrated in this study that T. cruzi infects human B cells, resulting in parasite-induced activation of caspase-7 followed by proteolytic cleavage of phospholipase Cgama1 and cell death. These data contribute to explain the mechanisms ruling B-cell depletion and evasion of the immune response by T. cruzi.
Texto completo:
1
Coleções:
06-national
/
BR
Base de dados:
SES-SP
/
SESSP-IBPROD
Idioma:
En
Revista:
Immunobiology
Ano de publicação:
2020
Tipo de documento:
Article