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Publication : Induction of T regulatory cells by cytotoxic T-lymphocyte antigen-2α on corneal endothelial cells.

First Author  Sugita S Year  2011
Journal  Invest Ophthalmol Vis Sci Volume  52
Issue  5 Pages  2598-605
PubMed ID  21245393 Mgi Jnum  J:171531
Mgi Id  MGI:4950326 Doi  10.1167/iovs.10-6322
Citation  Sugita S, et al. (2011) Induction of T Regulatory Cells by Cytotoxic T-Lymphocyte Antigen-2{alpha} on Corneal Endothelial Cells. Invest Ophthalmol Vis Sci 52(5):2598-605
abstractText  Purpose. To determine whether murine corneal endothelial (CE) cells can promote the generation of T regulatory (Treg) cells in vitro. Methods. To induce Treg cells in vitro by CE cell lines, T cells exposed to CE cells were used as Treg cells. T cells exposed to CE cells in the presence of anti-mouse CD3 antibody were harvested and added to target bystander T cells in vitro. T-cell activation was assessed for proliferation by [(3)H]-thymidine incorporation. Expression of CD25 or Foxp3 on Treg cells was evaluated by flow cytometry. Expression of cytotoxic T-lymphocyte antigen-2 alpha (CTLA-2alpha) on CE cells was evaluated by flow cytometry, RT-PCR, immunohistochemistry, or in situ hybridization. Anti-CTLA-2alpha neutralizing antibodies, CTLA-2alpha siRNA, or pro-cathepsin L blocking proteins were used to abolish the CE-inhibitory function. Results. Cultured CE cells produced CTLA-2alpha on their surfaces, thereby enabling bystander CD4(+) T cells to be converted to Treg cells by TGFbeta promotion. CE-induced Treg cells had immunosuppressive capacities by highly expressing CD25(high) and Foxp3. When mRNA downregulation (siRNA transfection), neutralizing antibodies, or blocking proteins were used to block CTLA-2alpha expression on CE cells, CE-induced Treg cells failed to acquire Treg function. Conclusions. These findings indicate that cell surface CTLA-2alpha contributes to the CE-dependent suppression of bystander T cells. Thus, ocular resident tissue-exposed T cells can be induced to become regulators within the peripheral microenvironment.
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