SciELO - Scientific Electronic Library Online

 
vol.67 número6Tratamiento de las neoplasias hematológicas en el embarazoLa ADN topoisomerasa tipo I de protozoos patógenos como Diana terapéutica de fármacos antitumorales índice de autoresíndice de assuntospesquisa de artigos
Home Pagelista alfabética de periódicos  

Serviços Personalizados

Journal

Artigo

Indicadores

  • Não possue artigos citadosCitado por SciELO

Links relacionados

  • Não possue artigos similaresSimilares em SciELO

Compartilhar


Medicina (Buenos Aires)

versão impressa ISSN 0025-7680versão On-line ISSN 1669-9106

Resumo

STEMPIN, Cinthia C  e  CERBAN, Fabio M. Macrophages and arginase induction as a mechanism for parasite escape. Medicina (B. Aires) [online]. 2007, vol.67, n.6, pp.737-746. ISSN 0025-7680.

Although there are several immunological mechanisms to eliminate the intracellular pathogens, they have elaborated a variety of strategies to escape of the immune response and to make possible their survival and replication in the host. Some parasites modulate the production of several toxic molecules synthesized by the immune system. Several parasites are highly sensitive to nitric oxide (ON) and their derivatives. ON is produced in macrophages (MΦ) after stimulation with microbial products or cytokines. In the past, M Φ were defined as inflammatory cells (classically activated MΦ), able to produce inflammatory mediators, to act like antigens presenting cells and to kill intracellular pathogens. Nevertheless, activated MΦ involve a more heterogeneous group of cells with different biological markers that can carry out different immunological functions. Alternatively activated MΦ fail to produce ON due to the arginase induction and consequently they have diminished their capacity to kill intracellular pathogens. It has been reported the induction of arginase by different parasites; therefore this mechanism could favor their survival in the host. In our group, we studied the participation of arginase in a model of Trypanosoma cruzi infection and the intracellular signals involved in the replication of this parasite in MΦ. The data obtained from our works would allow the understanding of some mechanisms by which cells can be programmed to favor the establishment of chronic parasitic infections.

Palavras-chave : Macrophages; Arginase; Parasite; MAPK; Ttrypanosoma cruzi.

        · resumo em Espanhol     · texto em Espanhol     · Espanhol ( pdf )

 

Creative Commons License Todo o conteúdo deste periódico, exceto onde está identificado, está licenciado sob uma Licença Creative Commons