Premium
Fas–FasL interaction modulates nitric oxide production in Trypanosoma cruzi ‐infected mice
Author(s) -
Martins Gislâine A.,
Petkova Stefka B.,
Machado Fabiana S.,
Kitsis Richard N.,
Weiss Louis M.,
Wittner Murray,
Tanowitz Herbert B.,
Silva João S.
Publication year - 2001
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1046/j.1365-2567.2001.01216.x
Subject(s) - fas ligand , trypanosoma cruzi , apoptosis , nitric oxide , cytokine , immune system , biology , immunology , fas receptor , nitric oxide synthase , interferon gamma , programmed cell death , endocrinology , biochemistry , parasite hosting , world wide web , computer science
Summary During acute Trypanosoma cruzi infection in mice, many leucocytes undergo apoptosis. Although apoptosis has been ascribed to increased levels of nitric oxide (NO) and Fas–FasL interaction, the importance of this phenomenon in modulating the host response against T. cruzi is unknown. Herein, the role of NO‐ and Fas–FasL‐induced apoptosis in modulating the immune response to T. cruzi was evaluated using mice deficient in Fas expression (MRL/MpJ‐Fas lpr ) and inducible nitric oxide synthase (iNOS) knockout mice (iNOS–/–). The results showed that besides decreasing apoptosis induction after infection, impairment of the Fas–FasL interaction resulted in decreased NO production, as a consequence of enhanced T helper 2 (Th2) cytokine production. Differently, blockage of NO‐induced apoptosis resulted in uncontrolled cytokine production, rather than a biased Th2 cytokine pattern. Together, these results suggested that Fas and FasL‐induced apoptosis could be implied in modulation of the immune response against T. cruzi by interfering with cytokine and NO production during the acute phase of the infection.