Critically, our integrated PB-derived secretome proteomics demonstrates that immunoactivating Tregs in CBIA preferentially secrete pro-inflammatory MCP1/MCP4, whereas RA immunoactivating Tregs produce the chemokines CCL11/CXCL10—functionally aligning with synovial fluid observations and underscoring disease-specific Treg polarization. The gene discussed is CCL2; the disease is rheumatoid arthritis.