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Trypanosoma brucei triggers a broad immune response in the adipose tissue

2021Journal article Open access
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dc.contributor.authorMachado, Henrique
dc.contributor.authorRebelo, Tiago
dc.contributor.authorSequeira, Mariana
dc.contributor.authorTrindade, Sandra
dc.contributor.authorCarvalho, Tânia
dc.contributor.authorRijo-Ferreira, Filipa
dc.contributor.authorRentroia-Pacheco, Barbara
dc.contributor.authorSerre, Karine
dc.contributor.authorFigueiredo, Luisa M.
dc.date.accessioned2021-09-28T15:31:02Z
dc.date.available2021-09-28T15:31:02Z
dc.date.issued2021
dc.descriptionCopyright: © 2021 Machado et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.pt_PT
dc.description.abstractAdipose tissue is one of the major reservoirs of Trypanosoma brucei parasites, the causative agent of sleeping sickness, a fatal disease in humans. In mice, the gonadal adipose tissue (AT) typically harbors 2-5 million parasites, while most solid organs show 10 to 100-fold fewer parasites. In this study, we tested whether the AT environment responds immunologically to the presence of the parasite. Transcriptome analysis of T. brucei infected adipose tissue revealed that most upregulated host genes are involved in inflammation and immune cell functions. Histochemistry and flow cytometry confirmed an increasingly higher number of infiltrated macrophages, neutrophils and CD4+ and CD8+ T lymphocytes upon infection. A large proportion of these lymphocytes effectively produce the type 1 effector cytokines, IFN-γ and TNF-α. Additionally, the adipose tissue showed accumulation of antigen-specific IgM and IgG antibodies as infection progressed. Mice lacking T and/or B cells (Rag2-/-, Jht-/-), or the signature cytokine (Ifng-/-) displayed a higher parasite load both in circulation and in the AT, demonstrating the key role of the adaptive immune system in both compartments. Interestingly, infections of C3-/- mice showed that while complement system is dispensable to control parasite load in the blood, it is necessary in the AT and other solid tissues. We conclude that T. brucei infection triggers a broad and robust immune response in the AT, which requires the complement system to locally reduce parasite burden.pt_PT
dc.description.sponsorshipThis work was supported by the European Research Council (FatTryp, ref. 771714) awarded to LMF, by Fundação para a Ciência e Tecnologia (CEECIND/03322/2018) awarded to LMF, (PTDC/MED-IMU/30948/2017 and CEECIND/00697/2018) awarded to KS, (PD/BD/128286/2017) awarded to HM, (SFRH/BPD/89833/2012) awarded to ST, (IMM/BI/83-2017 through PTDC/BIM-MET/4471/2014) awarded to TB-R and by the National Institutes of Health (NIGMS K99GM132557) awarded to FR-F. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationPLoS Pathog. 2021 Sep 15;17(9):e1009933pt_PT
dc.identifier.doi10.1371/journal.ppat.1009933pt_PT
dc.identifier.eissn1553-7374
dc.identifier.issn1553-7366
dc.identifier.urihttp://hdl.handle.net/10451/49665
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherPLOSpt_PT
dc.relationCEECIND/03322/2018pt_PT
dc.relationExploring the hidden life of African trypanosomes: parasite fat tropism and implications for disease
dc.relation.publisherversionhttps://journals.plos.org/plospathogens/pt_PT
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/pt_PT
dc.titleTrypanosoma brucei triggers a broad immune response in the adipose tissuept_PT
dc.typejournal article
dspace.entity.typePublication
oaire.awardTitleExploring the hidden life of African trypanosomes: parasite fat tropism and implications for disease
oaire.awardURIinfo:eu-repo/grantAgreement/EC/H2020/771714/EU
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/9471 - RIDTI/152174/PT
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/CEEC IND 2018/6764/PT
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/OE/59823/PT
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/OE/34847/PT
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/3599-PPCDT/143103/PT
oaire.citation.issue9pt_PT
oaire.citation.startPagee1009933pt_PT
oaire.citation.titlePLOS Pathogenspt_PT
oaire.citation.volume17pt_PT
oaire.fundingStreamH2020
oaire.fundingStream9471 - RIDTI
oaire.fundingStreamCEEC IND 2018
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oaire.fundingStream3599-PPCDT
person.familyNameMachado
person.familyNameRebelo
person.familyNameSequeira
person.familyNameTrindade
person.familyNameCarvalho
person.familyNameRijo-Ferreira
person.familyNameRentroia-Pacheco
person.familyNameSerre
person.familyNameFigueiredo
person.givenNameHenrique
person.givenNameTiago
person.givenNameMariana
person.givenNameSandra
person.givenNameTânia
person.givenNameFilipa
person.givenNameBarbara
person.givenNameKarine
person.givenNameLuisa M
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project.funder.identifierhttp://doi.org/10.13039/501100008530
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project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.nameEuropean Commission
project.funder.nameFundação para a Ciência e a Tecnologia
project.funder.nameFundação para a Ciência e a Tecnologia
project.funder.nameFundação para a Ciência e a Tecnologia
project.funder.nameFundação para a Ciência e a Tecnologia
project.funder.nameFundação para a Ciência e a Tecnologia
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT
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