Abstract
Regulatory T (Treg) cells require PTEN to block PI3K signaling while maintaining Foxp3 expression. In the absence of PTEN, Treg cells lose Foxp3 expression and their suppressive function, leading to a systemic increase in interferon-γ secretion, with consequent expansion of pathogenic T helper 1 and follicular B helper T cells and systemic autoimmunity.
MeSH terms
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Autoimmunity / genetics*
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Forkhead Transcription Factors / metabolism
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Homeostasis
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Humans
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Interleukin-2 / metabolism
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Interleukin-2 Receptor alpha Subunit / metabolism
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PTEN Phosphohydrolase / metabolism*
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Signal Transduction
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T-Lymphocytes, Regulatory / enzymology*
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T-Lymphocytes, Regulatory / immunology
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T-Lymphocytes, Regulatory / pathology*
Substances
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FOXP3 protein, human
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Forkhead Transcription Factors
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Interleukin-2
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Interleukin-2 Receptor alpha Subunit
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PTEN Phosphohydrolase