Expansion of CD25-Negative Forkhead Box P3-Positive T Cells during HIV and Mycobacterium tuberculosis Infection
| dc.contributor.author | Angerami, Matías T | |
| dc.contributor.author | Suarez, Guadalupe V | |
| dc.contributor.author | Vecchione, María B | |
| dc.contributor.author | Laufer, Natalia | |
| dc.contributor.author | Ameri, Diego | |
| dc.contributor.author | Ben, Graciela | |
| dc.contributor.author | Perez, Hector | |
| dc.contributor.author | Sued, Omar | |
| dc.contributor.author | Salomon, Horacio | |
| dc.contributor.author | Quiroga, María F | |
| dc.date.accessioned | 2024-05-23T23:50:02Z | |
| dc.date.available | 2024-05-23T23:50:02Z | |
| dc.date.issued | 2017-05-09 | |
| dc.description | Fil: Sued O. Fundación Huésped, Buenos Aires; Argentina | es_ES |
| dc.description.abstract | Tuberculosis (TB) and HIV alter the immune system, and coinfected (HIV-TB) individuals usually present deregulations of T-lymphocytic immune response. We previously observed an increased frequency of “unconventional” CD4+CD25−FoxP3+ Treg (uTreg) population during HIV-TB disease. Therefore, we aimed to explore the phenotype and function of uTreg and conventional CD4+CD25+FoxP3+ Treg subsets (cTreg) in this context. We evaluated the expression of CD39, programmed cell death protein 1 (PD1), glucocorticoid-induced tumor necrosis factor receptor (GITR), and the effector/memory distribution by flow cytometry in cTreg and uTreg. Also, IL-10, TGF-β, IFN-γ production, and the suppressor capacity of uTregs were analyzed in cocultures with effector lymphocytes and compared with the effect of regulatory T cells (Tregs). We found diminished expression of CD39 and higher levels of PD1 on uTreg compared to cTreg in both HIV-TB and healthy donors (HD). In addition, uTreg and cTreg showed differences in maturation status in both HIV-TB and HD groups, due to the expansion of effector memory uTregs. Interestingly, both HIV-TB and HD showed a pronounced production of IFN-γ in uTreg population, though no significant differences were observed for IL-10 and TGF-β production between uTreg and cTreg. Moreover, IFN-γ+ cells were restricted to the CD39− uTreg population. Finally, when the suppressor capacity was evaluated, both uTreg and cTreg inhibited polyclonal T cell-proliferation and IFN-γ production in a similar extent. These findings suggest that uTregs, which are expanded during HIV-TB coinfection, exert regulatory functions in a similar way to cTregs despite an altered surface expression of Treg characteristic markers and differences in cytokine production. | es_ES |
| dc.format | application/pdf | es_ES |
| dc.identifier.doi | https://doi.org/10.3389/fimmu.2017.00528 | |
| dc.identifier.uri | https://repositorio.huesped.org.ar/handle/123456789/1416 | |
| dc.language | ENG | es_ES |
| dc.provenance | Published | es_ES |
| dc.relation.ispartofseries | Front. Immunol;Volume 8 - 2017 | |
| dc.rights | openAccess | es_ES |
| dc.subject | HIV | es_ES |
| dc.title | Expansion of CD25-Negative Forkhead Box P3-Positive T Cells during HIV and Mycobacterium tuberculosis Infection | es_ES |
| dc.type | Documento de Conferencia | es_ES |