Effect of partial depletion of CD25+ T cells on neurological deficit and tissue damage in acute cerebral ischemia rat models

dc.creatorRodríguez Perea, Ana Lucía
dc.creatorGutiérrez Vargas, Johanna
dc.creatorRojas López, Mauricio
dc.creatorCardona Gómez, Gloria Patricia
dc.creatorVelilla Hernandez, Paula Andrea
dc.date2021-10-09T17:54:43Z
dc.date2021-10-09T17:54:43Z
dc.date2018
dc.date.accessioned2023-08-28T20:28:37Z
dc.date.available2023-08-28T20:28:37Z
dc.identifier2221-6189
dc.identifierhttp://hdl.handle.net/10495/23062
dc.identifier10.4103/2221-6189.248029
dc.identifier2589-5516
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/8479813
dc.descriptionABSTRACT: Objective: To evaluate the role of regulatory T cells (Tregs) at late stages of stroke. Methods: Anti-CD25 antibody (or PBS as a control) was injected to reduce the pool of Tregs in Wistar rats; then, ischemia was induced transiently by middle cerebral artery occlusion during 60 min and reperfusion was allowed for 7 d. Then, Treg frequency was analyzed in peripheral blood, spleen and lymph nodes. Neurological score (0-6) and infarct volume were also determined. Results: Nine days after injection, the CD4+ CD25+ T cells were reduced by 70.4%, 44.8% and 57.9% in peripheral blood, spleen and lymph nodes, respectively compared to PBS-treated rats. In contrast, the reduction of CD4+ FOXP3+ T cells was lower in the same compartments (38.6%, 12.5%, and 29.5%, respectively). The strongest reduction of CD25+ CD4+ T cells was observed in those FOXP3-negative cells in blood, spleen and lymph nodes (77.8%, 52.8%, and 60.7%, respectively), most likely corresponding to activated T cells. Anti-CD25-treated transient middle cerebral artery occlusion rats had a lower neurological deficit and did not develop tissue damage compared with PBS-treated animals. Conclusions: These findings suggest that treatment with anti-CD25 in our model preferentially reduce the T cell population with an activated phenotype, rather than the Treg population, leading to neuroprotection by suppressing the pathogenic response of effector T cells.
dc.descriptionCOL0070457
dc.descriptionCOL0012444
dc.descriptionCOL0010744
dc.descriptionCOL0008639
dc.format7
dc.formatapplication/pdf
dc.formatapplication/pdf
dc.languageeng
dc.publisherHainan Medical University
dc.publisherBacterias y Cáncer
dc.publisherGrupo de Inmunología Celular e Inmunogenética
dc.publisherGrupo de Neurociencias de Antioquia
dc.publisherInmunovirología
dc.publisherHaikou, China
dc.relationJ. Acute Dis.
dc.rightsinfo:eu-repo/semantics/openAccess
dc.rightshttp://creativecommons.org/licenses/by-nc-sa/2.5/co/
dc.rightshttp://purl.org/coar/access_right/c_abf2
dc.rightshttps://creativecommons.org/licenses/by-nc-sa/4.0/
dc.subjectIsquemia Encefálica
dc.subjectBrain Ischemia
dc.subjectLinfocitos T Reguladores
dc.subjectT-Lymphocytes, Regulatory
dc.subjectLinfocitos T
dc.subjectT-Lymphocytes
dc.subjectTransitory middle cerebral artery occlusion
dc.subjectRat
dc.subjectAnti-CD25
dc.titleEffect of partial depletion of CD25+ T cells on neurological deficit and tissue damage in acute cerebral ischemia rat models
dc.typeinfo:eu-repo/semantics/article
dc.typeinfo:eu-repo/semantics/publishedVersion
dc.typehttp://purl.org/coar/resource_type/c_2df8fbb1
dc.typehttps://purl.org/redcol/resource_type/ART
dc.typeArtículo de investigación


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