| Author | Campos, Marco Antônio Silva | |
| Author | Gazzinelli, Ricardo Tostes | |
| Access date | 2025-01-17T18:33:36Z | |
| Available date | 2025-01-17T18:33:36Z | |
| Document date | 2004 | |
| Citation | CAMPOS, Marco Antônio Silva; GAZZINELLI, Ricardo Tostes. Trypanosoma cruzi and its components, as exogenous mediators of inflammation recognized through Toll-like receptors. Mediators Inflamm., v. 13, n. 3, p. 139-143, 2004. | en_US |
| ISSN | 0962-9351 | en_US |
| URI | https://www.arca.fiocruz.br/handle/icict/68129 | |
| Language | eng | en_US |
| Publisher | Rapid Communications of Oxford Ltd | en_US |
| Rights | restricted access | |
| Subject in Portuguese | Trypanosoma cruzi | en_US |
| Subject in Portuguese | Doença de Chagas | en_US |
| Title | Trypanosoma cruzi and its components, as exogenous mediators of inflammation recognized through Toll-like receptors. | en_US |
| Type | Article | |
| DOI | 10.1080/09511920410001713565 | |
| Abstract | Trypanosoma cruzi is the etiologic agent of Chagas' disease, a parasitic disease of enormous importance in Latin America. Herein we review the studies that revealed the receptors from innate immunity that are involved in the recognition of this protozoan parasite. We showed that the recognition of T. cruzi and its components occurs through Toll-like receptors (TLR) 2/CD14. Further, we showed in vivo the importance of the myeloid differentiation factor (MyD88), an adapter protein essential for the function of TLRs, in determining the parasitemia and mortality rate of mice infected with T. cruzi. We also discuss the implications of these findings in the pathophysiology of Chagas' disease. | en_US |
| Affilliation | Fundação Oswaldo Cruz. Centro de Pesquisas René Rachou. Laboratório de Imunopatologia. Belo Horizonte, MG, Brasil. | en_US |
| Affilliation | Fundação Oswaldo Cruz. Centro de Pesquisas René Rachou. Laboratório de Imunopatologia. Belo Horizonte, MG, Brasil. | en_US |
| Subject | Trypanosoma cruzi | en_US |
| Subject | Chagas' disease | en_US |
| Embargo date | 2050-12-31 | |
