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Interleukin 2 signaling is required for CD4(+) regulatory T cell function.

Authors
  • Furtado, Gláucia C
  • Curotto de Lafaille, Maria A
  • Kutchukhidze, Nino
  • Lafaille, Juan J
Type
Published Article
Journal
The Journal of experimental medicine
Publication Date
Sep 16, 2002
Volume
196
Issue
6
Pages
851–857
Identifiers
PMID: 12235217
Source
Medline
License
Unknown

Abstract

Mice deficient in interleukin (IL)-2 production or the IL-2 receptor alpha or beta chains develop a lethal autoimmune syndrome. CD4(+) regulatory T cells have been shown to prevent autoimmune diseases, allograft rejection, and to down-regulate antibody responses against foreign antigens. To assess the role of IL-2 in the generation and function of regulatory T cells, we transferred CD4(+) T cells from mice genetically deficient in IL-2 or IL-2R(alpha) (CD25) expression. A small number of splenic or thymic CD4(+) T cells from IL-2 knockout mice can protect mice from spontaneous experimental autoimmune encephalomyelitis (EAE). In contrast, splenic or thymic CD4(+) T cells from CD25 knockout donor mice conferred little or no protection. We conclude that T cells with regulatory potential can develop, undergo thymic selection, and migrate to the peripheral lymphoid organs in the absence of IL-2, and do not protect from disease by means of IL-2 secretion. However, IL-2 signaling in regulatory T cells is essential for their protective function. Altogether, our results favor a model whereby IL-2 induces regulatory T cell activity.

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