Fig 1: Co-localization of ANXA1 and CD31 (A), integrin-α8 (B), synaptopodin (C), LTL (D), Calbindin D28K (E) and NE (F), CD68 (G), CD3 (H), CD4 (I) and CD8 (J) in renal specimens of AAV patients respectively. AAV, anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis; ANXA1, annexin A1; CD3, cluster of differentiation 3; CD4, cluster of differentiation 4; CD8, cluster of differentiation 8; CD31, cluster of differentiation 31; CD68, cluster of differentiation 68; LTL, lotus tetragonolobus lectin; NE, neutrophil elastase.
Fig 2: Splenic T cells take up PEG‐HCCs. As shown in (a), the T cell surface marker CD3 was used to isolate a purified population of T cells from vehicle and PEG‐HCC treated animals. These T cells were then assessed for the presence of PEG‐HCCs as shown in (b) Among PEG‐HCC‐treated samples, permeabilized samples had significantly higher PEG positive cells than what was observed in intact samples. n = 3 per group. *p < 0.05.
Fig 3: Accumulation of [Gd]DTPA‐PEG‐HCCs is seen in the lymph node cortex around the germination centers. [Gd]DTPA‐PEG‐HCCs (red) accumulate in the cortex, including the area surrounding germination centers within lymph nodes as shown in (a). This area is adjacent to the T‐cell zone as evidenced by positive CD3 staining (green). Positive [Gd]DTPA‐PEG‐HCC staining is absent in images taken from vehicle treated lymph nodes as shown in (b). All images are 20X magnification. A schematic of the lymph node is shown in (c) to indicate relevant regions where positive [Gd]DTPA‐PEG‐HCC staining was observed.
Fig 4: CBD reduces hepatic inflammation induced by CCl4. (A) Representative images of immunostaining for F4/80 (macrophage-specific marker; upper panel) and CD3 (lymphocyte-specific marker; bottom panel) from control, CCl4-vehicle, and CCl4 + CBD mice. Scale bars represent 100 μm. (B) Quantification of (percentage of total liver area) for F4/80 and CD3 (left and right panel respectively). Values are expressed as mean ± SEM (n = 6 animals per group). ***p < 0.001 vs. control group; ### p < 0.001 vs. CCl4 group (ANOVA followed by Tukey’s test).
Fig 5: Preferential localization of immune sequences in granulomas during infection with M. tuberculosis. a At 3, 8, and 12 weeks post M. tuberculosis infection (wpi), the fixed lung tissue sections were stained with hematoxylin–eosin (H&E) and signals for Cc10, Cd68, Inos, and Cd3e were plotted on DAPI labeling as background. Pseudo-color density XY positional log2 plots of transcript representations are shown below for Cd68, Inos, and Cd3e transcripts. One representative of three consecutive sections is displayed. Scale: 1000 μm. b The ratio of amplified transcripts in granulomas vs. unaffected regions was calculated for each transcript. The mean log2 ratio of transcript density in the granuloma in relation to the density in unaffected region + SEM in three consecutive sections is depicted. Sections from lungs at 3 and 12 wpi are compared. *Differences in relative transcript density at 3 and 12 wpi are significant (p < 0.05 unpaired Student’s t-test). Source data are provided as a Source Data file
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