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dc.contributor.authorFranco, D. de Lima
dc.contributor.authorNascimento, R. C.
dc.contributor.authorFerreira, K. S. [UNIFESP]
dc.contributor.authorAlmeida, S. R.
dc.identifier.citationScandinavian Journal of Immunology. Malden: Wiley-Blackwell, v. 75, n. 2, p. 142-146, 2012.
dc.description.abstractSporotrichosis is a chronic granulomatous mycosis caused by the dimorphic fungus Sporothrix schenckii. the immunological mechanisms involved in the prevention and control of sporotrichosis suggest that cell-mediated immunity plays an important role in protecting the host against S. schenckii. Nonetheless, recent data strongly support the existence of protective Abs against this pathogenic fungus. in a previous study, we showed that passive Ab therapy led to a significant reduction in the number of colony forming unit in the organs of mice when the MAb was injected before and during S. schenckii infection. the ability of opsonization to enhance macrophage damage to S. schenckii and subsequent cytokine production was investigated in this work. Here we show that the fungicidal characteristics of macrophages are increased when the fungus is phagocytosed in the presence of inactivated serum from mice infected with S. schenckii or mAb anti-gp70. Additionally, we show an increase in the levels of pro-inflammatory cytokines such as TNF-a and IL-1 beta. This study provides additional support for the importance of antibodies in protecting against S. schenckii and concludes that opsonization is an important process to increase TNF-a production and fungus killing by macrophages in experimental sporotrichosis.en
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.relation.ispartofScandinavian Journal of Immunology
dc.rightsAcesso aberto
dc.titleAntibodies Against Sporothrix schenckii Enhance TNF-a Production and Killing by Macrophagesen
dc.contributor.institutionUniversidade de São Paulo (USP)
dc.contributor.institutionUniversidade do Estado do Rio de Janeiro (UERJ)
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.description.affiliationUniv São Paulo, Fac Ciencias Farmaceut, Dept Anal Clin & Toxicol, BR-05508900 São Paulo, Brazil
dc.description.affiliationUniv Estado Rio de Janeiro, Inst Biol Roberto Alcantara Gomes, Lab Micol Celular & Prote, BR-20550011 Rio de Janeiro, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Dept Ciencias Biol, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Dept Ciencias Biol, São Paulo, Brazil
dc.description.sponsorshipIDFAPESP: 06/50472-2
dc.description.sourceWeb of Science

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