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EFEITO DO BLOQUEIO DO RECEPTOR DE IL-10 NA RESPOSTAIMUNE CONTRA Leishmania amazonensis.

by do Amaral, Joana Ferreira

Abstract (Summary)
The evaluation of the role of IL-10 in leishmaniasis is of extreme importance since this anti-inflammatory cytokine inhibits the action of IFN-? and NO, which play an important role in the elimination of the parasite and control of lesion development. In this study, the role of IL-10 in the infection by L.(L.) amazonensis was evaluated in vivo by treating infected C57Bl/6 mice with monoclonal antibodies against the IL-10 receptor (?-IL-10R) during the initial phase of the infection. Rat IgG was used as treatment control at the same dose used for the ?-IL-10R antibody (0.5 mg/animal/dose). Another group was left untreated. After three weeks, mice treated with ?-IL-10R presented histopathological profile, TNF production and parasite quantification similar to control animals. On the other hand, IFN-? production by lymph node cells from ?-IL-10R treated animals was higher than in control groups. No differences in course of infection, parasitism and cytokine production were observed between animals treated or not sacrificed at 12 weeks of infection. Histologically, a greater inflammatory infiltrate and an slightly increased tissue parasitism was observed in ?-IL-10R treated animals at this time point. Our data suggest that a different mechanism of evasion, other than induction of IL-10, are involved in the infection by L.(L.) amazonensis, since even in the presence of an increased IFN-? production the infection remains unchecked. The role of TGF-? induction by the parasite, as well as the resistance of L.(L.) amazonensis to NO in comparison to other Leishmania species are discussed.
This document abstract is also available in Portuguese.
Bibliographical Information:

Advisor:Luis Carlos Crocco Afonso; Marta de Lana; Kenneth John Gollob

School:Universidade Federal de Ouro Prêto

School Location:Brazil

Source Type:Master's Thesis

Keywords:Imunobiologia

ISBN:

Date of Publication:04/19/2002

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