Article Figures & Data
Figures
- Figure 1 Log10-fold changes of markers of T-cell exhaustion and senescence in samples from patients with IMNM
We did not observe statistically significant differences between patients with anti-SRP and anti-HMGCR autoantibodies. Statistical analysis was performed using Kruskal-Wallis one-way analysis of variance with Dunn multiple comparison test. HMGCR = hydroxy-3-methylglutaryl-coenzyme A reductase; SRP = signal recognition particle.
- Figure 2 Immunohistochemical stains of skeletal muscle biopsies from patients with IMNM, sIBM, or irMyositis
In IMNM biopsies, PD1+ cells are diffusely distributed in the endomysium (A) and most of them correspond to CD3+ T cells (D). Macrophages in myophagocytosis and endomysial macrophages are PD-L1+ (B) but the sarcolemma of myofibers is not (B). CD68 + macrophages coexpress PD-L2 (E), they colocalize with MHC class I+ sarcolemmal membranes (G), and PD1+ lymphocytes interact with PD-L2+ sarcolemmal structures (F) (A and C, original magnification ×200; B, original magnification ×400; D-F, original magnification ×600). In sIBM biopsies, PD1+ cells are CD3+, and they are detectable in the endomysium surrounding myofibers (H, K). PD-L1 is faintly detectable in macrophages within myophagocytosis but not on the sarcolemma and not on endomysial or perimysial macrophages (I). The sarcolemma of myofibers and macrophages are PD-L2+ and colocalize with sarcolemmal MHC class I (J, N). CD68 + macrophages coexpress PD-L2 (L), and PD1+ lymphocytes only occasionally interact with PD-L2+ sarcolemmal structures (M) (H-J, original magnification ×200; K-N, original magnification ×600). In irMyositis, PD1+ cells are detectable in the endomysium and they are CD3+ with variable intensity (O, R). PD-L1 is positive on macrophages but not all CD68 + macrophages express PD-L1 (P). The sarcolemma of myofibers is moderately PD-L2 positive (Q) and faintly coexpresses MHC class I (U). CD68 + macrophages interact with PD-L2+ sarcolemmal structures (S). Single PD1+ T cells interact with PD-L2 sarcolemmal structures (T) (O-Q, original magnification ×200; R-U original magnification ×600). IMNM = immune-mediated necrotizing myopathy; irMyositis = myositis induced by immune checkpoint inhibitors; sIBM = sporadic inclusion body myositis.
- Figure 3 Markers of T-cell exhaustion and senescence in patient skeletal muscle samples
mRNA levels of genes related to T-cell exhaustion (A and B) and T-cell senescence (C) from IMNM (n = 12), sIBM (n = 7), and irMyositis (n = 9) samples. Statistical analysis was performed using Kruskal-Wallis one-way analysis of variance with Dunn multiple comparison test. *p < 0.05; **p < 0.01; ***p < 0.001—difference between displayed groups in log fold changes. #p < 0.05; ##p < 0.01; ###p < 0.001—differences between dCT of patient groups and normal control. IMNM = immune-mediated necrotizing myopathy; irMyositis = myositis induced by immune checkpoint inhibitors; sIBM = sporadic inclusion body myositis.
- Figure 4 Markers of inflammation in IMNM (n = 42) and sIBM (n = 7) skeletal muscle samples
Markers for interstitial inflammation were upregulated in samples of IMNM and sIBM. All changes were significant at p < 0.01 compared to control samples (n = 8). TNFα and IFNγ levels differed significantly between IMNM and sIBM samples. Statistical analysis was performed using Kruskal-Wallis one-way analysis of variance with Dunn multiple comparison test. *p < 0.05—difference between displayed groups in log fold changes. IMNM = immune-mediated necrotizing myopathy; sIBM = sporadic inclusion body myositis.
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