Trypanosoma cruzi-induced suppression of human peripheral blood lymphocytes activated via the alternative (CD2) pathway.

AUTOR(ES)

Beltz, L A

RESUMO

Coculture of blood forms of Trypanosoma cruzi with human peripheral blood mononuclear cells stimulated with anti-CD2(2) and anti-CD2(3) monoclonal antibodies, i.e., via an antigen-independent pathway of T-lymphocyte activation, resulted in marked immunosuppression compared with that in parallel cultures in which parasites were absent. This effect was evidenced by a decreased lymphoproliferative capacity, a significant reduction in the proportion of cells expressing interleukin-2 receptors, and a significant diminution in the cell surface density of this receptor.

Documentos Relacionados

• Trypanosoma cruzi-induced immunosuppression: selective triggering of CD4+ T-cell death by the T-cell receptor-CD3 pathway and not by the CD69 or Ly-6 activation pathway.
• Role for Interleukin-1β in Trypanosoma cruzi-Induced Cardiomyocyte Hypertrophy
• Nitric oxide is involved in control of Trypanosoma cruzi-induced parasitemia and directly kills the parasite in vitro.
• Trypanosoma cruzi-induced immunosuppression: blockade of costimulatory T-cell responses in infected hosts due to defective T-cell receptor-CD3 functioning.
• Trypanosoma cruzi-induced host immune system dysfunction: a rationale for parasite immunosuppressive factor(s) encoding gene targeting