Characterization of chronic cutaneous lesions from TNF-receptor-1-deficient mice infected by Leishmania major.
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.
Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil.
Carolina Ferreira
CF
Oliveira
Daniel
D
Manzoni-de-Almeida
Paula Seixas
PS
Mello
Caio Cotta
CC
Natale
Helton da Costa
Hda C
Santiago
Luíza da Silva
Lda S
Miranda
Fernanda Oliveira
FO
Ferraz
Liliane Martins
LM
dos Santos
Mauro Martins
MM
Teixeira
Rosa Maria Esteves
RM
Arantes
Leda Quercia
LQ
Vieira
D000818:Animals; D017209:Apoptosis / Q000276:immunology; D016207:Cytokines / Q000276:immunology / Q000378:metabolism; D018320:Leishmania major / Q000276:immunology*; D016773:Leishmaniasis, Cutaneous / Q000235:genetics* / Q000276:immunology* / Q000469:parasitology; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D059208:Parasite Load; D047888:Receptors, Tumor Necrosis Factor, Type I / Q000172:deficiency* / Q000235:genetics
D016207:Cytokines; D047888:Receptors, Tumor Necrosis Factor, Type I