<p>R script for SHAP-based interpretation analysis.</p>

We identified 37 shared candidate genes between PD and sJIA, which were significantly enriched in IL‑17, NF‑κB, rheumatoid arthritis, and lipid atherosclerosis pathways, and machine learning screening further selected six core diagnostic genes (<i>FAM46C</i>, <i>CXCL1</i>, <i>SELP</i>, <i>LGALSL</i>, <i>ELOVL4</i>, <i>VCAN</i>), with <i>SELP</i> demonstrating the most robust cross‑model, cross‑dataset diagnostic value (AUC > 0.8); SHAP analysis confirmed <i>SELP</i> as a stable risk‑driving predictor across all models, while <i>CXCL1</i> consistently showed protective effects.

Immune infiltration revealed shared neutrophil elevation and CD8 ⁺ T‑cell reduction, with conserved <i>CXCL1</i> and <i>SELP</i> correlations with neutrophils and resting mast cells, and <i>FAM46C</i> with plasma cells.Drug‑target network analysis identified <i>IL1B, MMP</i>1, and <i>ITGAM</i> as core targets, and molecular docking yielded strong binding affinities for deoxycholic acid–<i>MMP1</i> (−7.6 kcal/mol), kaempferol–<i>IL1B</i> (−7.2 kcal/mol), kaempferol–<i>ITGAM</i> (−6.9 kcal/mol), with MD simulations confirming stable and specific binding.

Collectively, this study explores shared genetic and immunological characteristics between PD and sJIA, suggests that <i>SELP</i> may serve as a critical cross‑disease diagnostic biomarker, and offers novel insights into their pathogenesis and potential therapeutic targets that warrant further experimental validation.</p></div>