Data/hora: 01/06/2024 01:26:30

Provedor de dados: | 17
País: | United Kingdom
Título: | Immunity to self co-generates regulatory T cells
Autores: | James A. Dromey; Bo Han Lee; Helen E. Young; Stuart I. Mannering; Kent P. Jensen; Daniel J. Thearle; Spiros Fourlanos; Larissa Belov; Leonard C. Harrison.
Data: | 2008-04-08
Ano: | 2008
Palavras-chave: | Immunology.
Resumo: | 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-[gamma] 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.
Tipo: | Manuscript

Identificador:

http://precedings.nature.com/documents/1774/version/1

oai:nature.com:10101/npre.2008.1774.1

http://hdl.handle.net/10101/npre.2008.1774.1

Fonte: | Nature Precedings
Fonte: | Creative Commons Attribution 3.0 License