Table 1. Molecular mechanisms of low-dose IL-2 therapy in SLE.

SLE: Systemic Lupus Erythematosus, Tregs: Regulatory T cells, IL-2: Interleukin-2, IL-2R: Interleukin-2 receptor, JAK1: Janus kinase 1, JAK3: Janus kinase 3, STAT5: Signal transducer and activator of transcription 5, PI3K: Phosphoinositide 3-kinase, Akt: Protein kinase B, MAPK: Mitogen-activated protein kinase, Foxp3: Forkhead box P3, CTLA-4: Cytotoxic T-lymphocyte-associated protein 4, IL-10: Interleukin-10, IFN-γ: Interferon-gamma, IL-17: Interleukin-17, TNF-α: Tumor necrosis factor-alpha, NK cells: Natural killer cells

Molecular Mechanism	Description
Regulation of Tregs	IL-2 selectively expands and activates regulatory T cells (Tregs), which maintain immune tolerance.
JAK-STAT Pathway	IL-2 binds to IL-2R, activating JAK1 and JAK3, leading to STAT5 phosphorylation and promotion of Treg function.
PI3K-Akt Pathway	Enhances Treg survival and resistance to apoptosis, promoting cell survival and metabolic activity.
MAPK Pathway	Contributes to Treg proliferation and differentiation.
Enhancement of Treg Function	IL-2 increases expression of genes like Foxp3, CTLA-4, and IL-10, enhancing Treg suppressive activity.
Modulation of Cytokine Environment	Reduces pro-inflammatory cytokines (IFN-γ, IL-17, TNF-α) and promotes anti-inflammatory cytokines (IL-10).
Impact on Effector T Cells	Preferentially targets Tregs without significantly stimulating effector T cells, minimizing autoreactivity.
Influence on NK Cells and Dendritic Cells	Enhances NK cell cytotoxic activity and modulates dendritic cell antigen-presenting function.