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*
Instituto Oswaldo Cruz, FIOCRUZ (Fundaçao Oswaldo Cruz), and
Programa de Imunobiologia, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil
Activation-induced cell death (AICD) of CD4+ T
lymphocytes was described in infection with Trypanosoma
cruzi, but a role for AICD in modulating parasite spread in host
cells has not been investigated. In this study, replication of T.
cruzi in vitro in murine macrophage (M
) monolayers was
investigated. Long term (5 to 13 day) replication of infective
(trypomastigote) T. cruzi forms was blocked by supernatants
from activated (anti-TCR) CD4+ T cells of infected mice
or by rIFN-
. However, when CD4+ T cells from infected
mice were cocultured with M and activated by anti-TCR, marked
exacerbation of trypomastigote growth in M ensued. The deleterious
effect required contact between T cells and infected M. Both
anti-Fas and TCR activation killed a proportion of CD4+
T cells. Ly-6 activation did not induce AICD and did not exacerbate
parasite growth. However, Fas-mediated killing of T cells before Ly-6
activation led to exacerbated parasite growth. Although a minor
population, Fas-susceptible cells were the major source of IFN-
production by activated T cells. Addition of a neutralizing
anti-Fas ligand antibody blocked 50 to 60% of CD4+ T
cell AICD and reduced trypomastigote growth in T/M cocultures
stimulated by anti-TCR. The results demonstrate that in
CD4+ T cells from infected mice, the onset of AICD
selectively ablates IFN- production and up-regulates parasite
replication in M in vitro. These findings suggest a deleterious role
for AICD in T. cruzi infection.
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