| First Author | Martins GA | Year | 2001 |
| Journal | Immunology | Volume | 103 |
| Issue | 1 | Pages | 122-9 |
| PubMed ID | 11380700 | Mgi Jnum | J:69492 |
| Mgi Id | MGI:1934727 | Doi | 10.1046/j.1365-2567.2001.01216.x |
| Citation | Martins GA, et al. (2001) Fas-FasL interaction modulates nitric oxide production in Trypanosoma cruzi-infected mice. Immunology 103(1):122-9 |
| abstractText | 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. |
