Article
Schistosoma mansoni antigens alter the cytokine response in vitro during cutaneous leishmaniasis
Registro en:
BAFICA, A. M. B. et al. Schistosoma mansoni antigens alter the cytokine response in vitro during cutaneous leishmaniasis. Memórias do Instituto Oswaldo Cruz, v. 106, n. 7, p. 856-863, 2011.
0074-0276
Autor
Bafica, Aline Michelle Barbosa
Cardoso, Luciana Santos
Oliveira, Sérgio Costa
Loukas, Alex
Varela, Giuseppe Tittoni
Oliveira, Ricardo Riccio
Bacellar, Olívia
Carvalho Filho, Edgar Marcelino
Araújo, Maria Ilma
Resumen
Oliveira, Ricardo Riccio; Carvalho Filho, Edgar Marcelino de. “Documento produzido em parceria ou por autor vinculado à Fiocruz, mas não consta à informação no documento”. MCT/CNPq (479417/2008 3 universal) MIA, SCO and EMC are investigators supported by CNPq. Schistosoma mansoni infection or associated products are able to down-modulate the type 1 CD4+ T cell inflammatory response characteristic of autoimmune diseases. In this study, we evaluated how S. mansoni antigens altered the immune response that was induced by the soluble Leishmania antigen (SLA) from cutaneous leishmaniasis (CL) patients. Cytokines were measured from the supernatants of peripheral blood mononuclear cell cultures stimulated with SLA. This was performed using the sandwich enzyme linked immunosorbent assay technique in the presence or absence of S. mansoni recombinant antigens Sm29, SmTSP-2 and PIII. The addition of S. mansoni antigens to the cultures resulted in the reduction of interferon gamma (IFN-γ) levels in 37-50% of patients. Although to a lesser extent, the antigens were also able to decrease the production of tumour necrosis factor-alpha (TNF-α). We compared patients that either had or did not have reduction in IFN-γ and TNF-α production in cultures stimulated with SLA in the presence of S. mansoni antigens. We found that there was no significant difference in the levels of interleukin (IL)-10 and IL-5 in response to S. mansoni antigens between the groups. The antigens used in this study down-modulated the in vitro proinflammatory response induced by SLA in a group of CL patients through a currently undefined mechanism.