Benznidazole Treatment following Acute Trypanosoma cruzi Infection Triggers CD8+ T-Cell Expansion and Promotes Resistance to Reinfection
AUTOR(ES)
Olivieri, Bianca Perdigão
FONTE
American Society for Microbiology
RESUMO
Many studies have shed light on the mechanisms underlying both immunoprotection and immune dysregulation arising after Trypanosoma cruzi infection. However, little is known about the impact of benznidazole (N-benzyl-2-nitroimidazole acetamide), the drug available for clinical treatment of the infection, on the immune system in the infected host. In the present study we investigated the effect of benznidazole therapy on the lymphoid compartment during the course of experimental T. cruzi infection. Although amelioration of a variety of clinical and parasitological signs was observed in treated mice, amelioration of splenocyte expansion was not detected. Interestingly, this sustained splenomegaly observed in benznidazole-treated mice showed a preferential expansion of CD8+ T lymphocytes. Moreover, although benznidazole treatment blocked the expansion of recently activated CD4+ and CD8+ T cells seen in infected hosts, benznidazole treatment led to a selective expansion of effector and memory CD8+ T lymphocytes in association with a lower rate of apoptosis. In addition, the surviving treated animals were protected from reinfection. Together, these data suggest that, in addition to its well-known direct role in blocking parasite replication in vivo, benznidazole appears to directly affect immune regulation in T. cruzi-infected hosts.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=132750Documentos Relacionados
- Expansion of Protective CD8+ T-Cell Responses Driven by Recombinant Cytomegaloviruses
- Detailed Analysis of the CD8+ T-Cell Response following Adenovirus Vaccination
- An Optimized CD8+ T-Cell Response Controls Productive and Latent Gammaherpesvirus Infection
- CD4+ T cells are required to sustain CD8+ cytotoxic T-cell responses during chronic viral infection.
- Immune Activation and CD8+ T-Cell Differentiation towards Senescence in HIV-1 Infection
