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Masteller EL, Warner MR, Tang Q, et al. Expansion of functional endogenous antigen-specific CD4+CD25+ regulatory T cells from nonobese diabetic mice. J Immunol. 2005;175(5):3053-9doi: 10.4049/jimmunol.175.5.3053.
Masteller, E. L., Warner, M. R., Tang, Q., Tarbell, K. V., McDevitt, H., & Bluestone, J. A. (2005). Expansion of functional endogenous antigen-specific CD4+CD25+ regulatory T cells from nonobese diabetic mice. Journal of immunology (Baltimore, Md. : 1950), 175(5), 3053-9. https://doi.org/10.4049/jimmunol.175.5.3053
Masteller, Emma L, et al. "Expansion of functional endogenous antigen-specific CD4+CD25+ regulatory T cells from nonobese diabetic mice." Journal of immunology (Baltimore, Md. : 1950) vol. 175,5 (2005): 3053-9. doi: https://doi.org/10.4049/jimmunol.175.5.3053
Masteller EL, Warner MR, Tang Q, Tarbell KV, McDevitt H, Bluestone JA. Expansion of functional endogenous antigen-specific CD4+CD25+ regulatory T cells from nonobese diabetic mice. J Immunol. 2005 Sep 01;175(5):3053-9. doi: 10.4049/jimmunol.175.5.3053. PMID: 16116193.
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J Immunol. 2005 Sep 01;175(5):3053-9. doi: 10.4049/jimmunol.175.5.3053.

Expansion of functional endogenous antigen-specific CD4+CD25+ regulatory T cells from nonobese diabetic mice.

Journal of immunology (Baltimore, Md. : 1950)

Emma L Masteller, Matthew R Warner, Qizhi Tang, Kristin V Tarbell, Hugh McDevitt, Jeffrey A Bluestone

Affiliations

  1. Diabetes Center, Department of Medicine, University of California, San Francisco, CA 94143-0540, USA.

PMID: 16116193 DOI: 10.4049/jimmunol.175.5.3053

Abstract

CD4+CD25+Foxp3+ regulatory T cells (T(reg)) are critical for controlling autoimmunity. Evidence suggests that T(reg) development, peripheral maintenance, and suppressive function are dependent on Ag specificity. However, there is little direct evidence that the T(reg) responsible for controlling autoimmunity in NOD mice or other natural settings are Ag specific. In fact, some investigators have argued that polyclonal Ag-nonspecific T(reg) are efficient regulators of immunity. Thus, the goal of this study was to identify, expand, and characterize islet Ag-specific T(reg) in NOD mice. Ag-specific T(reg) from NOD mice were efficiently expanded in vitro using IL-2 and beads coated with recombinant islet peptide mimic-MHC class II and anti-CD28 mAb. The expanded Ag-specific T(reg) expressed prototypic surface markers and cytokines. Although activated in an Ag-specific fashion, the expanded T(reg) were capable of bystander suppression both in vitro and in vivo. Importantly, the islet peptide mimic-specific T(reg) were more efficient than polyclonal T(reg) in suppressing autoimmune diabetes. These results provide a direct demonstration of the presence of autoantigen-specific T(reg) in the natural setting that can be applied as therapeutics for organ-specific autoimmunity.

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