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Clinical and Developmental ImmunologyVolume 2012 2012, Article ID 865708, 12 pages

Research Article

Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Avenue Antonio Carlos 6627, 31270-901 Belo Horizonte, MG, Brazil

Núcleo de Pesquisa em Ciências Biológicas, Instituto de Ciências Biológicas e Exatas, Universidade Federal de Ouro Preto, Morro do Cruzeiro, 35400-000 Ouro Preto, MG, Brazil

Departamento de Patologia Geral, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Avenue Antonio Carlos 6627, 31270-901 Belo Horizonte, MG, Brazil

Received 15 July 2011; Accepted 28 August 2011

Academic Editor: Alfonso J. Rodriguez-Morales

Copyright © 2012 Carolina Ferreira Oliveira et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Leishmania major-infected TNF receptor 1 deficient TNFR1 KO mice resolve parasitism but fail to resolve lesions, while wild-type mice completely heal. We investigated the cell composition, cytokine production, and apoptosis in lesions from L. major-infected TNFR1 KO and wild-type WT mice. Chronic lesions from L. major-infected TNFR1 KO mice presented larger number of CD8+ T and Ly6G+ cells. In addition, higher concentrations of mRNA for IFN-γ CCL2 and CCL5, as well as protein, but lower numbers of apoptotic cells, were found in lesions from TNFR1 KO mice than in WT, at late time points of infection. Our studies showed that persistent lesions in L. major-infected TNFR1 KO mice may be mediated by continuous migration of cells to the site of inflammation due to the presence of chemokines and also by lower levels of apoptosis. We suggest that this model has some striking similarities to the mucocutaneous clinical form of leishmaniasis.





Autor: Carolina Ferreira Oliveira, Daniel Manzoni-de-Almeida, Paula Seixas Mello, Caio Cotta Natale, Helton da Costa Santiago, Luíz

Fuente: https://www.hindawi.com/



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