Publication
Association between EBV serological patterns and lymphocytic profile of SjS patients support a virally triggered autoimmune epithelitis
| dc.contributor.author | Barcelos, F | |
| dc.contributor.author | Martins, C | |
| dc.contributor.author | Monteiro, R | |
| dc.contributor.author | Cardigos, J | |
| dc.contributor.author | Prussiani, T | |
| dc.contributor.author | Sítima, M | |
| dc.contributor.author | Alves, N | |
| dc.contributor.author | Vaz-Patto, JA | |
| dc.contributor.author | Cunha-Branco, J | |
| dc.contributor.author | Borrego, LM | |
| dc.date.accessioned | 2021-02-26T23:23:05Z | |
| dc.date.available | 2021-02-26T23:23:05Z | |
| dc.date.issued | 2021-02-18 | |
| dc.description.abstract | Sjögren's syndrome (SjS) is characterized by lymphocytic infiltration of exocrine glands, i.e. autoimmune epithelitis. Lymphocytes are central in SjS pathogenesis, with B-cell hyperactivity mediated by T-cells. B-cells are main targets of Epstein-Barr virus (EBV) infection, a frequently-suggested trigger for SjS. We aimed to evaluate how the EBV infection modulates B and T-cell subsets in SjS, including as controls Rheumatoid arthritis patients (RA) and healthy participants (HC). SjS patients presented decreased CXCR5+T-cells, although IL21-secreting Tfh and Tfc cells were increased. Tfc were positively correlated with ESSDAI scores, suggesting their relevant role in SjS pathogenesis. As previously described, SjS patients showed expanded circulating naïve B-cell compartments. SjS patients had a higher incidence of EBV-EA-D-IgG+ antibodies, characteristic of recent EBV-infection/reactivation. SjS patients with past infection or recent infection/reactivation showed increased CXCR3+Th1 and CXCR3+Tfh1 cells compared to those without active infection. SjS patients with a recent infection/reactivation profile presented increased transitional B-cells compared to patients with past infection and increased plasmablasts, compared to those without infection. Our results suggest EBV-infection contributes to B and T-cell differentiation towards the effector phenotypes typical of SjS. Local lymphocyte activation at ectopic germinal centres, mediated by Tfh and Tfc, can be EBV-driven, perpetuating autoimmune epithelitis, which leads to gland destruction in SjS. | pt_PT |
| dc.description.version | info:eu-repo/semantics/publishedVersion | pt_PT |
| dc.identifier.citation | Sci Rep . 2021 Feb 18;11(1):4082. | pt_PT |
| dc.identifier.doi | 10.1038/s41598-021-83550-0 | pt_PT |
| dc.identifier.uri | http://hdl.handle.net/10400.26/35738 | |
| dc.language.iso | eng | pt_PT |
| dc.peerreviewed | yes | pt_PT |
| dc.subject | Síndrome de Sjogren | pt_PT |
| dc.subject | Sjogren's Syndrome | pt_PT |
| dc.title | Association between EBV serological patterns and lymphocytic profile of SjS patients support a virally triggered autoimmune epithelitis | pt_PT |
| dc.type | journal article | |
| dspace.entity.type | Publication | |
| oaire.citation.issue | 1 | pt_PT |
| oaire.citation.startPage | 4082 | pt_PT |
| oaire.citation.title | Scientific reports | pt_PT |
| oaire.citation.volume | 11 | pt_PT |
| rcaap.rights | openAccess | pt_PT |
| rcaap.type | article | pt_PT |
Files
Original bundle
1 - 1 of 1