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. 2020 Dec 1;11:6149. doi: 10.1038/s41467-020-19918-z

Fig. 1. Decrease in circulating pDCs in autoimmunity is independent of disease activity and therapy.

Fig. 1

a Gating strategy to identify the pDC population within PBMCs: pDCs are characterized by the lack of expression of lineage markers (CD3, CD19, CD56, CD14, CD11c), intermediate to high expression of HLA-DR, high expression of CD123 (IL-3R) and CD303 (BDCA-2). b Average percentage of pDCs in PBMCs of age- and sex-matched healthy controls (HC; n = 37), At-Risk individuals (At-Risk; n = 64), patients with systemic lupus erythematosus (SLE; n = 81) and primary Sjögren’s Syndrome (pSS; n = 21). cf Association between the percentage of pDCs in PBMCs and type I IFN activity in the blood (IFN score A) in HC, At-Risk, SLE, and pSS. g Percentage of pDCs in PBMCs in SLE patients with inactive and active disease. h Percentage of pDCs in PBMCs in SLE patients treated with or without hydroxychloroquine (HCQ). i Percentage of pDCs in PBMCs in SLE patients treated with other immunosuppressants (MTX = methotrexate, AZA = azathioprine, MMF = mycophenolate mofetil). j Association between the percentage of pDCs in PBMCs and the dose of prednisolone in patients with SLE. Data are represented as mean ± SEM. ns = not significant; ****P < 0.0001. Two-way ANOVA (b), nonlinear regression (cf and j), unpaired two-tailed t-test (gi).