title: Upregulation of CD94 on CD8+T cells in anterior chamber-associated immune deviation.
abstract: 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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Guangzhou, PR China. hehao3000@qq.com
authors.forename: Hao
authors.initials: H
authors.lastname: He
authors.forename: Peizeng
authors.initials: P
authors.lastname: Yang
authors.forename: Liqiong
authors.initials: L
authors.lastname: Jiang
authors.forename: Junfeng
authors.initials: J
authors.lastname: Zhang
authors.forename: Changlin
authors.initials: C
authors.lastname: Zhao
authors.forename: Lina
authors.initials: L
authors.lastname: Chen
authors.forename: Xiaomin
authors.initials: X
authors.lastname: Lin
authors.forename: Hongyan
authors.initials: H
authors.lastname: Zhou
authors.forename: Aize
authors.initials: A
authors.lastname: Kijlstra
mesh_terms: D000818:Animals; D000867:Anterior Chamber / Q000276:immunology*; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology* / Q000378:metabolism; D005260:Female; D051858:Forkhead Transcription Factors / Q000378:metabolism; D053804:Granzymes / Q000378:metabolism; D007108:Immune Tolerance; D007165:Immunosuppression Therapy; D051379:Mice; D008810:Mice, Inbred C57BL; D051920:NK Cell Lectin-Like Receptor Subfamily D / Q000276:immunology*; D054353:Perforin / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D011971:Receptors, Immunologic / Q000276:immunology / Q000378:metabolism*; D013154:Spleen / Q000276:immunology; D050378:T-Lymphocytes, Regulatory / Q000276:immunology* / Q000378:metabolism; D016212:Transforming Growth Factor beta / Q000276:immunology / Q000378:metabolism; D015854:Up-Regulation
chemical_list: D051858:Forkhead Transcription Factors; C498833:Foxp3 protein, mouse; D051920:NK Cell Lectin-Like Receptor Subfamily D; D012333:RNA, Messenger; D011971:Receptors, Immunologic; D016212:Transforming Growth Factor beta; D054353:Perforin; D053804:Granzymes