IL2RA antisense RNA 1 (IL2RA-AS1)

IL2RA antisense RNA 1 (IL2RA-AS1), also called LIRIL2R, is a long noncoding RNA transcribed in the locus of IL2RA but on the antisense strand. It plays a crucial regulatory role in human T cell biology, particularly in the differentiation and function of induced and natural regulatory T cells (iTregs and nTregs)[2]. LIRIL2R promotes IL2RA (CD25) and FOXP3 expression by binding chromatin upstream of the IL2RA promoter and affecting the local epigenetic landscape. Silencing of LIRIL2R leads to decreased IL2RA and FOXP3 expression, reduced STAT5 phosphorylation after IL-2 stimulation, and dysregulation of the Treg transcriptional program, which in turn impacts immune tolerance. Thus, IL2RA-AS1 acts as a key modulator of regulatory T cell identity and immune homeostasis. There is no evidence it is a receptor, transporter, enzyme, or direct therapeutic drug target, making it functionally classified as a regulatory RNA rather than a typical "target" in the classical pharmacological sense[2]. This entity is often confused with IL2RA (Interleukin-2 receptor alpha chain); IL2RA-AS1 does not encode a protein, is not a canonical cell surface receptor, and is not directly targeted by existing drugs. The main literature focus is on mechanistic immunology studies[2].

Other names

LIRIL2R (Long Intergenic RNA Induced by IL2RA Regulation)LOC105374869

Silencing of IL2RA-AS1 with antisense oligonucleotides affects IL2RA and FOXP3 levels, but no clinical pharmacological agents are established[2]. IL2RA-AS1 promotes IL2RA (CD25) and FOXP3 expression by binding chromatin upstream of the IL2RA promoter and affecting the local epigenetic landscape. Silencing leads to decreased IL2RA and FOXP3 expression, reduced STAT5 phosphorylation after IL-2 stimulation, and dysregulation of the Treg transcriptional program.