Th17 and regulatory T cells contribute to the in situ immune response in skin lesions of Jorge Lobo's disease

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dc.contributor Sistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP
dc.contributor.author KANASHIRO-GALO, Luciane FMUSP-HC
PAGLIARI, Carla FMUSP-HC
BARBOZA, Tania Cristina
BRITO, Arival Cardoso de
XAVIER, Marilia Brasil
OLIVEIRA, Clivia Maria Moraes de
UNGER, Deborah Aben Athar
SOTTO, Mirian Nacagami FMUSP-HC
QUARESMA, Juarez Antonio Simoes
DUARTE, Maria Irma Seixas FMUSP-HC
dc.date.issued 2016
dc.identifier.citation MEDICAL MYCOLOGY, v.54, n.1, p.23-28, 2016
dc.identifier.issn 1369-3786
dc.identifier.uri http://observatorio.fm.usp.br/handle/OPI/13427
dc.description.abstract Jorge Lobo's disease (JLD) is a chronic granulomatous mycosis described in various Latin American countries. The main objective of the present study was to investigate the possible role of Th17 and Foxp3+ Treg cells in the pathogenesis of Jorge Lobo's disease. Human skin biopsies were submitted to an immunohistochemistry protocol to detect Foxp3, interleukin (IL)-1beta, CD25, IL-6, IL-17, and IL-23. The epidermis presented acanthosis, hyperkeratosis, and frequent presence of fungi. The dermis presented inflammatory infiltrate comprising macrophages, lymphocytes, epithelioid and multinucleated cells, and an intense number of fungi. Foxp3+ Treg cells and IL-17+ cells were visualized in lymphocytes in the inflammatory infiltrate. IL-1, IL-2R (CD25), IL-6, and IL-23 were visualized in the dermis, intermingled with fungal cells, permeating or participating of the granuloma. Following IL-17, the most prominent cytokine was IL-6. IL-23 and cells expressing CD25 were present in fewer number. The comparative analysis between IL-17 and Foxp3 demonstrated a statistically significant increased number of IL-17+ cells. Th17 cells play a role in the immune response of JLD. IL-1beta and IL-6 added to the previously described increased number of TGF-beta would stimulate such pattern of response. Th17 cells could be present as an effort to modulate the local immune response; however, high levels of a Th17 profile could overcome the role of Treg cells. The unbalance between Treg/Th17 cells seems to corroborate with the less effective immune response against the fungus.
dc.description.sponsorship · CNPq [470512/2013-0]
· Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES)
dc.language.iso eng
dc.publisher OXFORD UNIV PRESS
dc.relation.ispartof Medical Mycology
dc.rights restrictedAccess
dc.subject Jorge Lobo's Disease; immune response; Th17 cells; regulatory T cells
dc.subject.other growth-factor-beta; lacazia-loboi; differentiation; lobomycosis; induction; effector; lineage; state
dc.title Th17 and regulatory T cells contribute to the in situ immune response in skin lesions of Jorge Lobo's disease
dc.type article
dc.rights.holder Copyright OXFORD UNIV PRESS
dc.description.group LIM/06
dc.description.group LIM/53
dc.identifier.doi 10.1093/mmy/myv069
dc.identifier.pmid 26333354
dc.type.category original article
dc.type.version publishedVersion
hcfmusp.author KANASHIRO-GALO, Luciane:HC:ICHC
hcfmusp.author PAGLIARI, Carla:FM:MPT
hcfmusp.author SOTTO, Mirian Nacagami:FM:MDT
hcfmusp.author DUARTE, Maria Irma Seixas:FM:MPT
hcfmusp.author.external · BARBOZA, Tania Cristina:Univ Sao Paulo, Fac Med, Lab Disciplina Patol Molestias Transmissiveis, Sao Paulo, SP, Brazil; Inst Assistencia Med Serv Publ Estadual, Programa Posgrad Ciencias Saude, Sao Paulo, SP, Brazil
· BRITO, Arival Cardoso de:Fed Univ Para, Nucleo Med Trop, BR-66059 Belem, Para, Brazil
· XAVIER, Marilia Brasil:Fed Univ Para, Nucleo Med Trop, BR-66059 Belem, Para, Brazil; Univ Estado Para, Belem, Para, Brazil
· OLIVEIRA, Clivia Maria Moraes de:Fed Univ Para, Nucleo Med Trop, BR-66059 Belem, Para, Brazil
· UNGER, Deborah Aben Athar:Fed Univ Para, Nucleo Med Trop, BR-66059 Belem, Para, Brazil
· QUARESMA, Juarez Antonio Simoes:Fed Univ Para, Nucleo Med Trop, BR-66059 Belem, Para, Brazil; Univ Estado Para, Belem, Para, Brazil
hcfmusp.origem.id WOS:000369984900002
hcfmusp.origem.id 2-s2.0-84971505644
hcfmusp.publisher.city OXFORD
hcfmusp.publisher.country ENGLAND
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dc.description.index MEDLINE
dc.identifier.eissn 1460-2709
hcfmusp.citation.scopus 4
hcfmusp.affiliation.country Brasil
hcfmusp.scopus.lastupdate 2021-07-23


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