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Upregulation of CD94 on CD8(+)T Cells in Anterior Chamber-Associated Immune Deviation

BACKGROUND: CD8(+ )regulatory T cells (Treg) have been considered to be involved in a model of ocular-induced tolerance, known as anterior chamber-associated immune deviation (ACAID). The phenotype and characteristics of CD8(+)Treg in ACAID remain only poorly understood. Recent studies have reported...

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Detalles Bibliográficos
Autores principales: He, Hao, Yang, Peizeng, Jiang, Liqiong, Zhang, Junfeng, Zhao, Changlin, Chen, Lina, Lin, Xiaomin, Zhou, Hongyan, Kijlstra, Aize
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2008
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2566975/
https://www.ncbi.nlm.nih.gov/pubmed/18816417
http://dx.doi.org/10.1186/1471-2172-9-53
Descripción
Sumario:BACKGROUND: CD8(+ )regulatory T cells (Treg) have been considered to be involved in a model of ocular-induced tolerance, known as anterior chamber-associated immune deviation (ACAID). The phenotype and characteristics of CD8(+)Treg in ACAID remain only poorly understood. Recent studies have reported that the CD94-Qa-1 system is implicated in the induction of ACAID CD8(+)Treg, but the functions and characteristics of CD8(+)CD94(+)T cells remain unclear. RESULTS: Both mRNA and protein of CD94 and NKG2A were markedly up-regulated on splenic CD8(+)T cells of ACAID mice compared with controls. Flow cytometric analysis showed that very few CD8(+)CD94(+)T cells express granzyme B, perforin and Foxp3. CD8(+)CD94(+)T cells, but not CD8(+)CD94(-)T cells, magnetically isolated from the spleens of ACAID mice, produced large amounts of TGF-beta1 and exhibited suppressive activity in vitro. Neutralization of TGF-beta1 caused reversal of suppression mediated by CD8(+)CD94(+)T cells. CONCLUSION: CD8(+)CD94(+)T cells from ACAID mice exhibited suppressive activity in association with enhanced expression of TGF-beta1, suggesting that CD8(+)Treg are mainly distributed in CD94(+)T cell subpopulations.