Fig 2: Correlation between serum PGLYRP2 and lipid metabolism indexes in SLE patients. (A) SLEDAI was positively correlated with LDL-c (r = 0.47, P < 0.01), Apo-B (r = 0.4524, P < 0.01), and Apo B/A1(r = 0.4015, P < 0.01) in SLE patients. (B) Serum PGLYRP2 was negatively correlated with HDL-c (r = 0.3746, P < 0.05) and Apo-A1 (r = 0.4523, P < 0.01), but positively correlated with Apo-B/A1 (r = 0.3.74, P < 0.05) in SLE patients

Fig 3: PGLYRP2 level increased in SLE patients. (A) Serum level of PGLYRP2 was significantly higher in SLE patients with stable disease (4468.99 ± 457.02 pg/ml), and those with active LN (5152.93 ± 446.13 pg/ml) or NP-SLE (5141.52 ± 579.61 pg/ml), than that healthy volunteers (3938.56 ± 576.07 pg/ml). (B) PGLYRP2 level in PBMCs was significantly higher in SLE patients with active LN or NP-SLE than that of healthy volunteers. (C) Receiver operating characteristic (ROC) curves showed that serum PGLYRP2 was capable of distinguishing SLE patients with active disease from those with stable disease (AUC = 0.841, 95%CI = 0.722–0.960, P = 0.000). *P < 0.05, ** < 0.01, ****P < 0.0001

Fig 4: Correlation between serum PGLYRP2 and disease activity of SLE. (A) Serum PGLYRP2 was significantly higher in high disease activity group (SLEDAI ⩾15, 5299.94 ± 570.87 pg/ml) than that in low disease activity group (SLEDAI⩽9, 4610.64 ± 533.59 pg/ml). (B) Serum level of PGLYRP2 was positively correlated with SLEDAI in SLE patients (r = 0.5783, P < 0.01)