IL2 encodes interleukin-2, a cytokine produced by activated CD4+ helper T cells and, to a lesser extent, activated CD8+ T cells and natural killer (NK) cells. IL-2 binds to either a high-affinity trimeric IL-2 receptor complex (IL2RA/CD25, IL2RB/CD122, IL2RG/CD132) or a low-affinity dimeric receptor (IL2RB and IL2RG), triggering JAK1 and JAK3 phosphorylation followed by STAT5 activation and downstream signaling through STAT, PI3K, and MAPK pathways. The cytokine functions as a T-cell growth factor, increases NK-cell cytolytic activity, promotes B-cell proliferation and immunoglobulin production, and plays a pivotal role in regulatory T-cell survival and proliferation—essential for immune tolerance. IL-2 also regulates effector T-cell differentiation, including Th1, Th2, and Th17 subsets, and supports memory CD8+ T-cell homeostasis 1. Loss of IL-2 responsiveness contributes to T-cell exhaustion during chr4 infections and tumor responses. Clinically, recombinant IL-2 can induce durable, complete regressions in patients with metastatic melanoma and renal cancer 2, and engineered IL-2 variants are being developed to improve efficacy while reducing systemic toxicity in cancer immunotherapy. IL-2-based approaches also extend to adoptive cell transfer and chimeric antigen receptor T-cell therapies 2.