Results: 3

1.
F <span style="font-variant: small-caps" class="small-caps">ig</span> . 3.

F ig . 3. From: Active systemic lupus erythematosus is associated with failure of antigen-presenting cells to express programmed death ligand-1.

Lupus flare APC express positive co-stimulatory molecules. PBMC were cultured for 1 day and gated for APC as given earlier. Compared with control cells (top row), SLE flare APC (middle row) lacked PD-L1 and the CD80/86hi subset of mDC. In contrast, SLE remission cells (bottom row) expressed both PD-L1 and CD80/86 in a pattern similar to that of controls (numbers in each graph represent the percentage of cells in each quadrant). Results are representative of two separate experiments using PBMC from three healthy controls, two SLE flare and two SLE remission.

N. Mozaffarian, et al. Rheumatology (Oxford). 2008 September;47(9):1335-1341.
2.
F <span style="font-variant: small-caps" class="small-caps">ig</span> . 1.

F ig . 1. From: Active systemic lupus erythematosus is associated with failure of antigen-presenting cells to express programmed death ligand-1.

Primary human PBMC spontaneously up-regulate PD-L1 protein. (A) Cells were cultured for 1 day and live PBMC gated by forward and side scatter. Histograms show mean fluorescence intensity (MFI) of PD-L1 as measured on CD3+ and CD3 cells from a healthy paediatric control (top), from a patient in SLE flare (middle) and from the same patient during SLE remission (bottom). (B) Using control PBMC, PD-L1+ cells were further characterized and found to separate into two groups based on CD14 expression. (C) Using antibodies to phenotypic markers, the PD-L1+ CD14lo and CD14hi cells were identified as immature mDC and Mo, respectively.

N. Mozaffarian, et al. Rheumatology (Oxford). 2008 September;47(9):1335-1341.
3.
F <span style="font-variant: small-caps" class="small-caps">ig</span> . 2.

F ig . 2. From: Active systemic lupus erythematosus is associated with failure of antigen-presenting cells to express programmed death ligand-1.

PD-L1 protein is deficient on APC during SLE flare, but not during remission. (A) PBMC were cultured for 1 day and APC subsets identified. (B) PD-L1 expression on both mDC and Mo was reduced during SLE flare, but not during remission. (C) CD1c staining demonstrated that PD-L1 expression in CD14lo CD11c+ cells was enriched on Type I immature mDC. (D) PD-L1 levels on mDC (upper graph) and Mo (lower graph) from 15 controls, 12 SLE flare and 14 SLE remission. Circles represent individual PD-L1 values and bars represent the mean MFI (±1 s.d.) for each group. For SLE flare mDC, *P < 6.5 × 10−3 compared with controls; #P < 2.5 × 10−2 compared with remission. For SLE flare Mo, *P < 1.8 × 10−4 compared with controls; #P < 2.4 × 10−6 compared with remission. For SLE remission Mo, *P < 3.4 ×10−3 compared with controls. (E) PD-L1 expression on mDC and Mo was normalized to background levels using the PD-L1 MFI of CD14 CD11c cells as the denominator for each sample. For SLE flare mDC, *P < 4.1 × 10−3 compared with controls; #P < 2.1 × 10−2 compared with remission. For SLE flare Mo, *P < 2.0 × 10−6 compared with controls; #P < 1.1 × 10−8 compared with remission. (F) SLE flare patients exhibited a lower percentage of PD-L1+ APC (mDC, upper graph and Mo, lower graph). For SLE flare mDC, *P < 4.2 × 10−3 compared with controls. For SLE flare Mo, *P < 1.1 ×10−6 compared with controls; #P < 4.0 ×10−8 compared with remission. (G) Mo PD-L1 values from (E) were graphed for patients with serial blood samples; shaded area denotes the ‘normal range’ of Mo PD-L1 expression observed in healthy controls (mean ± 1 s.d.).

N. Mozaffarian, et al. Rheumatology (Oxford). 2008 September;47(9):1335-1341.

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