#4-42E. The Dual Role of IL-2 in Systemic Lupus Erythematosus: A Balancing Act (Cytokine, 2025)

How can a single cytokine both drive and suppress inflammation in complex autoimmune diseases like systemic lupus erythematosus (SLE)? This review explores the paradoxical role of interleukin-2 (IL-2) in SLE pathogenesis, detailing how it amplifies inflammation by activating effector T cells and natural killer cells, while simultaneously being essential for maintaining immune tolerance through the expansion of regulatory T cells (Tregs). The critical clinical insight of this paper is that low-dose IL-2 therapy can selectively expand Tregs to restore immune homeostasis without triggering pathogenic effector cells. However, when critically appraising this approach, clinicians must consider the potential risk of inadvertently stimulating autoreactive effector cells and the practical treatment challenges posed by the extremely short in vivo half-life of conventional IL-2. For physicians, understanding this dual mechanism is highly relevant; it paves the way for optimizing precision medicine in SLE, offering actionable insights into emerging targeted therapeutics and the refinement of individualized disease management in daily clinical practice.

Citation: Hao Li, Jing He. The dual role of IL-2 in systemic lupus erythematosus: balancing pro-inflammatory and anti-inflammatory effects. Cytokine. 2025. DOI: 10.1016/j.cyto.2025.157032

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