IKZF4

IKZF4/Eos is a zinc-finger transcription factor of the Ikaros family that binds GGGAA Ikaros recognition sites and functions as a transcriptional repressor^[1]. In FOXP3⁺ regulatory T cells, Eos directly interacts with Foxp3 and induces chromatin modifications that silence target genes, making IKZF4 relevant to Treg programming, immune tolerance, and gene repression assays^[2]. Mechanistically, IKZF4 belongs to the Treg signature gene set, and Treg-specific epigenetic programs help maintain stable expression of genes such as Ikzf2 and Ikzf4 beyond transient FoxP3 expression^[3]. In disease models, selective Eos deletion in Treg cells caused loss of suppressive function and systemic autoimmunity, supporting IKZF4-focused autoimmune research designs^[4]. Compared with the related isoform IKZF2/Helios, Eos and Helios are both highly expressed in CD4⁺ Treg cells, yet double-deficient models showed unimpaired Treg development and distinct, largely non-overlapping transcriptional programs^[5]. Eos downregulation also controlled reprogramming of an Eos-labile Foxp3⁺ T-helper subset at inflammatory sites^[6]. Outside Treg biology, Eos regulated IL-2 and Th17 production in CD4⁺ conventional T cells and promoted TH2 differentiation through STAT5 activity^[7][8]. For experimental applications, the CELMoD degrader BMS-986449 degrades IKZF2/IKZF4 and supports Treg-reprogramming studies in solid tumor models^[9].