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Immunity to self co-generates regulatory T cells

James A. Dromey¹, Bo Han Lee¹, Helen E. Young¹, Stuart I. Mannering¹, Kent P. Jensen¹, Daniel J. Thearle¹, Spiros Fourlanos¹, Larissa Belov² & Leonard C. Harrison¹

Correspondence: (Login to view email address)

1. The Walter and Eliza Hall Institute of Medical Research, Autoimmunity & Transplantation Division
2. Medsaic Pty. Ltd.

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Document Type:

Manuscript

Date:

Received 08 April 2008 23:43 UTC; Posted 09 April 2008

Subjects:

Immunology

Tags:

• regulatory T cells
• immune regulation
• type 1 diabetes
• autoimmunity
• tolerance

Abstract:

Immune responses to self are kept in check by tolerance mechanisms, including suppression by regulatory T cells (Tregs). The defective generation of Tregs specific for self-antigens may lead to autoimmune disease. We identified a novel population of human CD4⁺ Tregs, characterized by high surface expression of CD52, which is co-generated in response to autoantigen. Blood CD4⁺CD52^hi T cells were generated preferentially in response to low-dose autoantigen and suppressed proliferation and interferon-γ production by other T cells. Depletion of resting CD4⁺CD52^hi T cells enhanced the T-cell response to autoantigen. CD4⁺CD52^hi Tregs were neither derived from nor distinguished by markers of conventional resting CD4⁺CD25⁺ Tregs. In response to the pancreatic islet autoantigens glutamic acid decarboxylase, the generation of CD4⁺CD52^hi Tregs was impaired in individuals with and at-risk for type 1 diabetes, compared to healthy controls and individuals with type 2 diabetes. CD4⁺CD52^hi Tregs co-generated to self-antigen may therefore contribute to immune homeostasis and protect against autoimmune disease.

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This document is licensed to the public under the Creative Commons Attribution 3.0 License

How to cite this document:

Dromey, James, Lee, Bo Han, Young, Helen, Mannering, Stuart, Jensen, Kent, Thearle, Daniel, Fourlanos, Spiros, Belov, Larissa, and Harrison, Leonard. Immunity to self co-generates regulatory T cells. Available from Nature Precedings <http://hdl.handle.net/10101/npre.2008.1774.1> (2008)

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