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Please use this identifier to cite or link to this item: http://hdl.handle.net/1843/58676
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dc.creatorRicardo Gonçalvespt_BR
dc.creatorKajal Hamidzadehpt_BR
dc.creatorDavid Mosserpt_BR
dc.date.accessioned2023-09-14T19:10:27Z-
dc.date.available2023-09-14T19:10:27Z-
dc.date.issued2020-
dc.citation.volume2pt_BR
dc.citation.issue4pt_BR
dc.citation.spage100046pt_BR
dc.citation.epage6pt_BR
dc.identifier.doihttps://doi.org/10.1016/j.cytox.2020.100046pt_BR
dc.identifier.issn2590-1532pt_BR
dc.identifier.urihttp://hdl.handle.net/1843/58676-
dc.description.resumoLeishmaniasis can present as a “spectrum” of clinical outcomes. There is evidence that these divergent clinical outcomes are attributable to genetic differences in the human host [1] as well the species of infecting parasite [2]. The spectrum of disease has largely been described by defining the polar opposites of T cell immune responses. In the mouse model, a TH1 immune response is associated with low numbers of Leishmania parasites in lesions, whereas a TH2 immune response has been associated with unrestricted parasite growth. In the present work, we revisit leishmaniasis and seek to better define the clinical spectrum as a function of divergent humoral immune responses. We describe examples in human, canine, and even some murine models of leishmaniasis that reveal a direct correlation between high anti-parasite antibody responses and unrestricted parasite growth. Therefore, we propose that the spectral nature of this disease may be due to quantitative and qualitative differences in the antibodies that are produced during disease. In human visceral leishmaniasis, a decrease in anti-parasite antibody levels may actually predict disease resolution. Thus, rather than defining this disease as a simple TH1/TH2 dichotomy, we propose that clinical leishmaniasis depends on the degree of humoral immunity, with high IgG predicting parasite persistence. These observations have obvious implications for vaccine development in leishmaniasis, and they may extend to other diseases caused by intracellular pathogens.pt_BR
dc.description.sponsorshipFAPEMIG - Fundação de Amparo à Pesquisa do Estado de Minas Geraispt_BR
dc.format.mimetypepdfpt_BR
dc.languageengpt_BR
dc.publisherUniversidade Federal de Minas Geraispt_BR
dc.publisher.countryBrasilpt_BR
dc.publisher.departmentICB - DEPARTAMENTO DE PATOLOGIApt_BR
dc.publisher.initialsUFMGpt_BR
dc.relation.ispartofCytokine: Xpt_BR
dc.rightsAcesso Abertopt_BR
dc.subjectLeishmaniapt_BR
dc.subjectVaccinept_BR
dc.subjectDTHpt_BR
dc.subjectHumoral immunitypt_BR
dc.subjectIgGpt_BR
dc.subject.otherLeishmaniapt_BR
dc.subject.otherVacinaspt_BR
dc.subject.otherImunidade Humoralpt_BR
dc.subject.otherImunoglobulina Gpt_BR
dc.titleHumoral immunity in leishmaniasis - prevention or promotion of parasite growth?pt_BR
dc.typeArtigo de Periódicopt_BR
dc.url.externahttps://www.sciencedirect.com/science/article/pii/S2590153220300264?via%3Dihubpt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-1127-4483pt_BR
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