CD4 Th1 but not Th2 clones efficiently activate macrophages to eliminate Trypanosoma cruzi through a nitric oxide dependent mechanism.

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 Lett

journal_title

Immunology letters

authors

Rodrigues MM,Ribeirão M,Boscardin SB

doi

10.1016/s0165-2478(00)00205-4

subject

Has Abstract

pub_date

2000-07-03 00:00:00

pages

43-50

issue

1

eissn

0165-2478

issn

1879-0542

pii

S0165-2478(00)00205-4

journal_volume

73

pub_type

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