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Medicina (Buenos Aires)

versión impresa ISSN 0025-7680versión On-line ISSN 1669-9106


STEMPIN, Cinthia C  y  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.

Palabras clave : Macrophages; Arginase; Parasite; MAPK; Ttrypanosoma cruzi.

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