Abstract:
:We have recently generated CD4 clones from BALB/c mice immunized with a plasmid DNA containing the gene encoding for the catalytic domain of trans-sialidase, an important enzyme expressed on the surface of Trypanosoma cruzi trypomastigotes. These clones allowed us to study in vitro the interaction between T cells and T. cruzi-infected macrophages. A cytotoxic CD4 clone of the Th1 type effectively activated macrophages to kill intracellular amastigote forms of T. cruzi. In contrast, CD4 Th2-like clones were much less efficient, being unable to activate macrophages to significantly reduce parasite development. We found that the anti-parasitic activity of Th1 cells was completely suppressed by the presence of nitric oxide synthase inhibitors. Also, we observed that anti-IFN-gamma antibodies significantly inhibited the anti-parasitic activity of these cells. We conclude that trypomastigote-specific Th1 cells activate macrophages to kill intracellular amastigotes of T. cruzi by a mechanism exclusively dependent on the induction of nitric oxide synthesis.
journal_name
Immunol Lettjournal_title
Immunology lettersauthors
Rodrigues MM,Ribeirão M,Boscardin SBdoi
10.1016/s0165-2478(00)00205-4subject
Has Abstractpub_date
2000-07-03 00:00:00pages
43-50issue
1eissn
0165-2478issn
1879-0542pii
S0165-2478(00)00205-4journal_volume
73pub_type
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