Abstract
Regulatory T (Treg) cells that express the signature transcription factor Foxp3 safeguard against autoimmunity and immune pathology. Recent studies show that a signaling network with the components phosphatidyl inositol 3 kinase (PI3K), Akt, and the mammalian target of rapamycin (mTOR) regulates the de novo expression of Foxp3 in CD4 T cells. In addition to CD4 T cell differentiation, PI3K/Akt/mTOR signaling also controls T cell migration. Here we review the new data, consider their evolutionary context and discuss their potential implications for immunotherapy.
MeSH terms
-
Animals
-
Cell Differentiation / drug effects*
-
Cell Differentiation / immunology
-
Cell Movement / genetics
-
Cell Movement / physiology
-
Food
-
Gene Expression Regulation / physiology
-
Growth Inhibitors / chemistry
-
Growth Inhibitors / pharmacology*
-
Humans
-
Immunotherapy / methods
-
Immunotherapy / trends
-
Models, Biological
-
Oncogene Protein v-akt / physiology
-
Phosphatidylinositol 3-Kinases / physiology
-
Protein Kinases / physiology
-
Receptors, Antigen, T-Cell / physiology
-
Signal Transduction / physiology
-
T-Lymphocytes, Regulatory / drug effects*
-
T-Lymphocytes, Regulatory / physiology*
-
TOR Serine-Threonine Kinases
Substances
-
Growth Inhibitors
-
Receptors, Antigen, T-Cell
-
Protein Kinases
-
MTOR protein, human
-
Oncogene Protein v-akt
-
TOR Serine-Threonine Kinases