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<MSIGDB BUILD_DATE="Jan 29, 2026" VERSION="2026.1.Hs" NAME="export">
    <GENESET STANDARD_NAME="ONO_FOXP3_TARGETS_UP" SYSTEMATIC_NAME="M1981" HISTORICAL_NAMES="" PMID="17377532" AUTHORS="Ono M,Yaguchi H,Ohkura N,Kitabayashi I,Nagamura Y,Nomura T,Miyachi Y,Tsukada T,Sakaguchi S" GEOID="" EXACT_SOURCE="Fig. S7: FOXP3, red" GENESET_LISTING_URL="" EXTERNAL_DETAILS_URL="" CHIP="MOUSE_GENE_SYMBOL" CONTRIBUTOR="Jessica Robertson" CONTRIBUTOR_ORG="MSigDB Team" DESCRIPTION_BRIEF="Genes up-regulated in CD4+ [GeneID=920] T lymphocytes transduced with FOXP3 [GeneID=50943]." DESCRIPTION_FULL="Naturally arising CD25+CD4+ regulatory T cells (T(R) cells) are engaged in the maintenance of immunological self-tolerance and immune homeostasis by suppressing aberrant or excessive immune responses, such as autoimmune disease and allergy. T(R) cells specifically express the transcription factor Foxp3, a key regulator of T(R)-cell development and function. Ectopic expression of Foxp3 in conventional T cells is indeed sufficient to confer suppressive activity, repress the production of cytokines such as interleukin-2 (IL-2) and interferon-gamma (IFN-gamma), and upregulate T(R)-cell-associated molecules such as CD25, cytotoxic T-lymphocyte-associated antigen-4, and glucocorticoid-induced TNF-receptor-family-related protein. However, the method by which Foxp3 controls these molecular events has yet to be explained. Here we show that the transcription factor AML1 (acute myeloid leukaemia 1)/Runx1 (Runt-related transcription factor 1), which is crucially required for normal haematopoiesis including thymic T-cell development, activates IL-2 and IFN-gamma gene expression in conventional CD4+ T cells through binding to their respective promoters. In natural T(R) cells, Foxp3 interacts physically with AML1. Several lines of evidence support a model in which the interaction suppresses IL-2 and IFN-gamma production, upregulates T(R)-cell-associated molecules, and exerts suppressive activity. This transcriptional control of T(R)-cell function by an interaction between Foxp3 and AML1 can be exploited to control physiological and pathological T-cell-mediated immune responses." TAGS="" MEMBERS="Ccr2,Ccr5,Ccr7,CD38,Cd97,Crem,Cxcr3,Ddx5,Dlk1,Folr4,Fos,Gadd45b,Gpr83,Gzmc,Il10,Itgae,Jun,Mecp2,Pak1,Pdcd1lg2,Rgs2,Slamf7,Socs2,Tnfrsf18" MEMBERS_SYMBOLIZED="ADGRE5,CCR2,CCR5,CCR7,CREM,CXCR3,DDX5,DLK1,FOS,GADD45B,GPR83,GZMB,IL10,ITGAE,IZUMO1R,JUN,MECP2,PAK1,PDCD1LG2,RGS2,SLAMF7,SOCS2,TNFRSF18" MEMBERS_EZID="10888,1234,1236,1390,1655,2353,2833,3002,3586,3682,3725,390243,4204,4616,5058,57823,5997,729230,80380,8784,8788,8835,976" MEMBERS_MAPPING="CD38,null,null|Ccr2,CCR2,729230|Ccr5,CCR5,1234|Ccr7,CCR7,1236|Cd97,ADGRE5,976|Crem,CREM,1390|Cxcr3,CXCR3,2833|Ddx5,DDX5,1655|Dlk1,DLK1,8788|Folr4,IZUMO1R,390243|Fos,FOS,2353|Gadd45b,GADD45B,4616|Gpr83,GPR83,10888|Gzmc,GZMB,3002|Il10,IL10,3586|Itgae,ITGAE,3682|Jun,JUN,3725|Mecp2,MECP2,4204|Pak1,PAK1,5058|Pdcd1lg2,PDCD1LG2,80380|Rgs2,RGS2,5997|Slamf7,SLAMF7,57823|Socs2,SOCS2,8835|Tnfrsf18,TNFRSF18,8784" FILTERED_BY_SIMILARITY="" FOUNDER_NAMES="" REFINEMENT_DATASETS="" VALIDATION_DATASETS="" CATEGORY_CODE="C2" ORGANISM="Mus musculus" SUB_CATEGORY_CODE="CGP"/>
</MSIGDB>
