Abstract
The inflammatory response in cutaneous leishmaniasis (CL), although responsible for controlling the infection, is associated with the pathogenesis of disease. Conversely, the immune response induced by S. mansoni antigens is able to prevent immune-mediated diseases. The aim of this study was to evaluate the potential of the S. mansoni Sm29 antigen to change the profile of monocyte-derived dendritic cells (MoDCs) from subjects with cutaneous leishmaniasis (CL) in vitro. Monocytes derived from the peripheral blood mononuclear cells of twelve patients were cultured with GM-CSF and IL-4 for differentiation into dendritic cells and then stimulated with soluble Leishmania antigen (SLA) in the presence or absence of Sm29 antigen. The expression of surface molecules associated with maturation and activation (HLA-DR, CD40, CD83, CD80, and CD86), inflammation (IL-12, TNF), and downregulation (IL-10, IL-10R) was evaluated using flow cytometry. We observed that the frequencies of HLA-DR, CD83, CD80, and CD86 as well as of IL-10 and IL-10R on MoDCs were higher in cultures stimulated with Sm29, compared to the unstimulated cell cultures. Our results indicate that the Sm29 antigen is able to activate regulatory MoDCs in patients with cutaneous leishmaniasis. It might be useful to control the inflammatory process associated with this disease.
Highlights
Leishmaniasis is endemic in 88 countries with approximately 12 million people infected and 350 million at risk worldwide, with an incidence of 1.5 million cases per year [1, 2]
These findings have provided the rationale for the use of recombinant S. mansoni proteins in in vitro studies with cells from patients with leishmaniasis in an attempt to modulate the inflammatory response associated with pathogenesis
Previous studies performed by our group have shown that the addition of the S. mansoni antigens Sm29, PIII, and TSP2 in cultured PBMC from cutaneous leishmaniasis patients stimulated with soluble Leishmania antigen (SLA) caused a reduction in the levels of IFN-γ and TNF in a significant number of individuals, with an increase in the levels of IL-10 [9]
Summary
Leishmaniasis is endemic in 88 countries with approximately 12 million people infected and 350 million at risk worldwide, with an incidence of 1.5 million cases per year [1, 2]. Studies have shown that chronic helminths infections, especially Schistosoma mansoni, possess the ability to BioMed Research International modulate the inflammatory response associated with both Th1 [7, 9] and Th2 [8, 11,12,13] immune-mediated diseases. These findings have provided the rationale for the use of recombinant S. mansoni proteins in in vitro studies with cells from patients with leishmaniasis in an attempt to modulate the inflammatory response associated with pathogenesis. The aim of this study was to evaluate the potential of the S. mansoni antigen Sm29 to induce a regulatory profile in monocytederived dendritic cells (MoDCs) from individuals with CL in an attempt to prevent or minimize the inflammatory response associated with the disease
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