title: Induced regulatory T-cells (iTregs) generated by activation with anti-CD3/CD28 antibodies differ from those generated by the physiological-like activation with antigen/APC.
abstract: Regulatory T-cells (Tregs) are responsible for homeostasis of the immune system, as well as for inhibition of pathogenic autoimmune processes. Induced-(i)-Tregs, can be generated in vitro by activation of CD4 cells in the presence of TGF-β. A commonly used activation mechanism is by antibodies against CD3 and CD28. The physiological-like activation of T-cells, however, is with the specific target antigen presented by antigen-presenting cells (APC). The two modes of activation have been considered to yield the same populations of iTregs. Here, we compared between iTreg populations generated by either one of the two methods and found differences between their capacities to inhibit T-lymphocyte proliferative response, their expression of cell surface antigens and particularly, in their transcript expression profiles of certain chemokines and chemokine receptors. Our data thus indicate that iTregs generated by activation with anti-CD3/CD28 antibodies cannot be considered identical to iTregs generated by antigen/APC.
authors.affiliation: Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD, United States; Department of Ophthalmology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
authors.forename: Chan
authors.initials: C
authors.lastname: Zhao
authors.affiliation: Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD, United States.
authors.forename: Guangpu
authors.initials: G
authors.lastname: Shi
authors.affiliation: Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD, United States.
authors.forename: Barbara P
authors.initials: BP
authors.lastname: Vistica
authors.affiliation: Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD, United States.
authors.forename: Samuel J H
authors.initials: SJ
authors.lastname: Hinshaw
authors.affiliation: Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD, United States.
authors.forename: Wambui S
authors.initials: WS
authors.lastname: Wandu
authors.affiliation: Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD, United States.
authors.forename: Cuiyan
authors.initials: C
authors.lastname: Tan
authors.affiliation: Department of Ophthalmology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China. Electronic address: meifen_zhang@hotmail.com.
authors.forename: Meifen
authors.initials: M
authors.lastname: Zhang
authors.affiliation: Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD, United States. Electronic address: geryi@nei.nih.gov.
authors.forename: Igal
authors.initials: I
authors.lastname: Gery
mesh_terms: D000818:Animals; D000938:Antigen-Presenting Cells / Q000276:immunology; D018106:CD28 Antigens / Q000276:immunology; D017252:CD3 Complex / Q000276:immunology; D016207:Cytokines / Q000096:biosynthesis; D005434:Flow Cytometry; D066298:In Vitro Techniques / Q000379:methods*; D008213:Lymphocyte Activation / Q000276:immunology*; D051379:Mice; D008822:Mice, Transgenic; D016133:Polymerase Chain Reaction; D016176:T-Lymphocyte Subsets / Q000276:immunology*; D050378:T-Lymphocytes, Regulatory / Q000276:immunology*
chemical_list: D018106:CD28 Antigens; D017252:CD3 Complex; D016207:Cytokines
keywords: Cell adhesion molecules; Proliferation assay; T cell activation; T regulatory (Treg) cells; TCR transgenic