Altered adaptive and TNF-superfamily soluble inflammatory mediators mark impending Systemic Lupus Erythematosus disease flare in European-American lupus patients after influenza vaccination (P6282)

Abstract

Abstract SLE is a waxing and waning disease characterized by major organ involvement, disease flares and immune dysregulation. Understanding mechanisms and identifying biomarkers of flare would help prevent damage and improve management. Plasma samples were obtained from SLE patients on the day of influenza vaccination (BL) and at 6 and 12 weeks post (FU) in 28 European American SLE patients who exhibited SELENA-SLEDAI defined disease flare at 6 (n=13) or 12 (n=15) weeks post-vaccination. Each SLE patient was matched to a unique SLE patient who did not flare (NF), and to a healthy control (HC). Samples from 13 SLE patients with flare were compared to samples from a non-flare year (self nonflare, SNF). Plasma samples were tested for 52 soluble inflammatory mediators using xMAP technology. SLE patients who exhibited disease flare had significantly (p < 0.01) higher levels of BL pro-inflammatory mediators, including Th1, Th2, and Th17-type cytokines compared to NF/SNF SLE patients and HC. Regulatory cytokines, including IL-10 and TGF-β were increased (p < 0.01) at BL in SLE patients not exhibiting disease flare (NF/SNF) compared to SLE flare and HC. TNFR family members, TNFRI, TNFRII, Fas, FasL, CD40L, were increased at BL in SLE flare patients. Select serum cytokines and chemokines are elevated in patients before SLE disease flare, providing important pathways to dissect for mechanism of flare, therapeutic selection or development.