Amastigotes of Trypanosoma cruzi express surface proteins that, when r
eleased into the host cell cytoplasm, are processed and presented on t
he surface of infected cells in the contest of MHC class I molecules t
o be recognized by CD8(+) CTL. To further understand the role of CTL i
n T. cruzi infection, we used the available MHC class I peptide bindin
g moths to identify potential CTL target epitopes in two recently desc
ribed T. cruzi amastigote surface proteins, ASP-1 and ASP-2, The predi
cted amino acid sequences of ASP-1 and ASP-2 were screened for H-2(b)
allele-specific class I peptide moths, and four peptides (PA11, PA12,
PA13, and PA14) and six peptides (PA5, PA6, PA7, PA8, PA9, and PA10) w
ere synthesized from ASP-1 and ASP-2, respectively. The majority of th
e peptides bound to some degree to H-2(b) class I MHC molecules, and s
is of 10 of the peptides stimulated spleen cells from T. cruzi-infecte
d mice to lyse target cells sensitized with the homologous peptides, S
hort term T cell lines specific for three of these peptides also lysed
T. cruzi-infected target cells. These results demonstrate that ASP-1
and ASP-2 are targets of in vivo generated CTLs and that this CTL resp
onse induced by T. cruzi infection is parasite and peptide specific, M
HC restricted, and CD8 dependent.