Regulatory T cells control strain specific resistance to Experimental Autoimmune Prostatitis

Breser, Maria L.; Lino, Andreia C.; Motrich, Ruben D.; Godoy, Gloria J.; Demengeot, Jocelyne; Rivero, Virginia E.

Publication

Regulatory T cells control strain specific resistance to Experimental Autoimmune Prostatitis

2016-09-14Journal article

dc.contributor.author	Breser, Maria L.
dc.contributor.author	Lino, Andreia C.
dc.contributor.author	Motrich, Ruben D.
dc.contributor.author	Godoy, Gloria J.
dc.contributor.author	Demengeot, Jocelyne
dc.contributor.author	Rivero, Virginia E.
dc.date.accessioned	2016-09-22T11:30:01Z
dc.date.available	2016-09-22T11:30:01Z
dc.date.issued	2016-09-14
dc.description	This deposit is composed by a publication in which the IGC' authors have had the role of collaboration (it's a collaboration publication). This type of deposit in ARCA is in restrictedAccess (it can't be in open access to the public), and could only be accessed by two ways: either by requesting a legal copy to the author (the email contact present in this deposit) or by visiting the following link: https://www.nature.com/articles/srep33097	pt_PT
dc.description.abstract	Susceptibility to autoimmune diseases results from the encounter of a complex and long evolved genetic context with a no less complex and changing environment. Major actors in maintaining health are regulatory T cells (Treg) that primarily dampen a large subset of autoreactive lymphocytes escaping thymic negative selection. Here, we directly asked whether Treg participate in defining susceptibility and resistance to Experimental Autoimmune Prostatitis (EAP). We analyzed three common laboratory strains of mice presenting with different susceptibility to autoimmune prostatitis upon immunization with prostate proteins. The NOD, the C57BL/6 and the BALB/c mice that can be classified along a disease score ranging from severe, mild and to undetectable, respectively. Upon mild and transient depletion of Treg at the induction phase of EAP, each model showed an increment along this score, most remarkably with the BALB/c mice switching from a resistant to a susceptible phenotype. We further show that disease associates with the upregulation of CXCR3 expression on effector T cells, a process requiring IFNγ. Together with recent advances on environmental factors affecting Treg, these findings provide a likely cellular and molecular explanation to the recent rise in autoimmune diseases incidence.	pt_PT
dc.description.sponsorship	Argentinean Agency for Promotion of Science and Technology; CONICET; National University of Córdoba grants; Cooperation Program in Science & Technology between Argentina and Portugal FCT–MINCYT.	pt_PT
dc.identifier.citation	Breser, M. L. et al. Regulatory T cells control strain specific resistance to Experimental Autoimmune Prostatitis. Sci. Rep. 6, 33097; doi: 10.1038/srep33097 (2016).	pt_PT
dc.identifier.doi	10.1038/srep33097	pt_PT
dc.identifier.uri	http://hdl.handle.net/10400.7/697
dc.language.iso	eng	pt_PT
dc.peerreviewed	yes	pt_PT
dc.publisher	Nature Publishing Group	pt_PT
dc.relation.publisherversion	http://www.nature.com/articles/srep33097	pt_PT
dc.rights.uri	http://creativecommons.org/licenses/by/4.0/	pt_PT
dc.subject	Autoimmunity	pt_PT
dc.subject	Immunological disorders	pt_PT
dc.title	Regulatory T cells control strain specific resistance to Experimental Autoimmune Prostatitis	pt_PT
dc.type	journal article
dspace.entity.type	Publication
oaire.citation.endPage	12	pt_PT
oaire.citation.startPage	1	pt_PT
oaire.citation.title	Scientific Reports	pt_PT
oaire.citation.volume	6	pt_PT
rcaap.rights	restrictedAccess	pt_PT
rcaap.type	article	pt_PT