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In vivo photoacoustic imaging and analysis of the vulnerability of atherosclerotic plaque. ( A - G ) Ex vivo distribution of <t>HMCN@Cy5.5</t> , Scr-HMCN@Cy5.5 , and OPN-HMCN@Cy5.5 in various organs—specifically the aorta ( B ), heart ( C ), liver ( D ), spleen ( E ), lung ( F ), and kidney ( G )—from apoE −/− mice at 0, 6, 12, and 24 h post-intravenous injection (n = 3). ( H ) Confocal images demonstrate the colocalization of OPN with CY5.5-labeled nanoparticles in aortic roots (n = 6, scale bars, 200 μm). ( I ) Quantitative analysis of the relative MFI of OPN and CY5.5 in different treatment groups. ( J , K ) Photoacoustic images and quantitative analysis of signal intensities of atherosclerotic plaque in carotid arteries of both healthy and atherosclerosis mice (n = 3). For each animal, longitudinal PA imaging was performed on the same carotid artery at predefined anatomical landmarks across different time points. Photoacoustic images were acquired with depth calibration based on acoustic time-of-flight measurements, converting ultrasound echo delay into depth using the predefined sound velocity in soft tissue. A calibrated depth scale bar is shown in each image, with an effective imaging depth of approximately 7 mm. ( L , M ) Pathological staining of atherosclerotic plaques in the carotid artery and aortic arch includes ORO and Masson staining (scale bar = 200 μm), as well as α -SMA, and CD68 fluorescent staining (scale bar = 100 μm each). ( N - Q ) The statistical analysis of ( N ) ORO staining (namely the percentage of LD area), ( O ) Masson staining (namely the percentage of collagen fiber area), ( P ) α -SMA fluorescent staining (namely the percentage of smooth muscle cell area) and ( Q ) CD68 fluorescent staining (namely the percentage of macrophage-derived foam cell area). ( R ) Vulnerability scores of aortic arch and carotid artery plaques. ∗ P < 0.05, ∗∗ P < 0.01, and ∗∗∗∗ P < 0.0001.
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In vivo photoacoustic imaging and analysis of the vulnerability of atherosclerotic plaque. ( A - G ) Ex vivo distribution of <t>HMCN@Cy5.5</t> , Scr-HMCN@Cy5.5 , and OPN-HMCN@Cy5.5 in various organs—specifically the aorta ( B ), heart ( C ), liver ( D ), spleen ( E ), lung ( F ), and kidney ( G )—from apoE −/− mice at 0, 6, 12, and 24 h post-intravenous injection (n = 3). ( H ) Confocal images demonstrate the colocalization of OPN with CY5.5-labeled nanoparticles in aortic roots (n = 6, scale bars, 200 μm). ( I ) Quantitative analysis of the relative MFI of OPN and CY5.5 in different treatment groups. ( J , K ) Photoacoustic images and quantitative analysis of signal intensities of atherosclerotic plaque in carotid arteries of both healthy and atherosclerosis mice (n = 3). For each animal, longitudinal PA imaging was performed on the same carotid artery at predefined anatomical landmarks across different time points. Photoacoustic images were acquired with depth calibration based on acoustic time-of-flight measurements, converting ultrasound echo delay into depth using the predefined sound velocity in soft tissue. A calibrated depth scale bar is shown in each image, with an effective imaging depth of approximately 7 mm. ( L , M ) Pathological staining of atherosclerotic plaques in the carotid artery and aortic arch includes ORO and Masson staining (scale bar = 200 μm), as well as α -SMA, and CD68 fluorescent staining (scale bar = 100 μm each). ( N - Q ) The statistical analysis of ( N ) ORO staining (namely the percentage of LD area), ( O ) Masson staining (namely the percentage of collagen fiber area), ( P ) α -SMA fluorescent staining (namely the percentage of smooth muscle cell area) and ( Q ) CD68 fluorescent staining (namely the percentage of macrophage-derived foam cell area). ( R ) Vulnerability scores of aortic arch and carotid artery plaques. ∗ P < 0.05, ∗∗ P < 0.01, and ∗∗∗∗ P < 0.0001.
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Coralite Dental Products cy5
BAITs enhance antigen uptake and digestion by DCs under TGFβ stimulation. (A) Schematic illustration of real-time DC migration assay. BAITs in the lower chamber create a chemokine gradient to attract DCs from the upper chamber. (B) Kinetics of DC migration measured as cell index (n = 3; n.s. is P > 0.05, ∗∗∗∗ is P < 0.0001 by two-way ANOVA with Bonferroni post-hoc test). (C) Crystal violet staining of non-migrated DCs (upper chamber) and Calcein-AM staining of migrated DCs (lower chamber) showing enhanced DC recruitment by BAITs. (D) The antigen uptake efficiency of DCs under varying antigen concentrations with or without TGFβ (n = 5; ∗∗∗ is P < 0.001, ∗∗∗∗ is P < 0.0001 by two-way ANOVA with Bonferroni post-hoc test). (E) Heatmap of immune-related genes in DCs showing upregulation of antigen presentation and co-stimulation markers and downregulation of suppressive factors as antigen concentration increases. (F) Antigen digestion capacity of DCs assessed in the presence or absence of TGFβ (n = 8; ∗∗∗∗ is P < 0.0001 by two-tailed Student's t -test). (G) Fluorescent images showing enhanced antigen uptake in DCs mediated by BAITs (quantified on right; n = 10; ∗∗∗∗ is P < 0.0001 by two-way ANOVA with Bonferroni post-hoc test). (H) Flow cytometry analysis of antigen-positive (Cy3 + ) DCs after incubation with free antigen or BAIT (quantified on right; n = 4; ∗∗∗∗ is P < 0.0001 by two-way ANOVA with Bonferroni post-hoc test). (I) BAITs improve antigen digestion and uptake of DCs under TGFβ stimulation. DCs were first incubated with <t>Cy5-antigens</t> for 12 h, followed by medium replacement and subsequent treatment with Cy3-antigens or Cy3-BAITs for an additional 6 h. Data are presented as mean ± SD.
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BAITs enhance antigen uptake and digestion by DCs under TGFβ stimulation. (A) Schematic illustration of real-time DC migration assay. BAITs in the lower chamber create a chemokine gradient to attract DCs from the upper chamber. (B) Kinetics of DC migration measured as cell index (n = 3; n.s. is P > 0.05, ∗∗∗∗ is P < 0.0001 by two-way ANOVA with Bonferroni post-hoc test). (C) Crystal violet staining of non-migrated DCs (upper chamber) and Calcein-AM staining of migrated DCs (lower chamber) showing enhanced DC recruitment by BAITs. (D) The antigen uptake efficiency of DCs under varying antigen concentrations with or without TGFβ (n = 5; ∗∗∗ is P < 0.001, ∗∗∗∗ is P < 0.0001 by two-way ANOVA with Bonferroni post-hoc test). (E) Heatmap of immune-related genes in DCs showing upregulation of antigen presentation and co-stimulation markers and downregulation of suppressive factors as antigen concentration increases. (F) Antigen digestion capacity of DCs assessed in the presence or absence of TGFβ (n = 8; ∗∗∗∗ is P < 0.0001 by two-tailed Student's t -test). (G) Fluorescent images showing enhanced antigen uptake in DCs mediated by BAITs (quantified on right; n = 10; ∗∗∗∗ is P < 0.0001 by two-way ANOVA with Bonferroni post-hoc test). (H) Flow cytometry analysis of antigen-positive (Cy3 + ) DCs after incubation with free antigen or BAIT (quantified on right; n = 4; ∗∗∗∗ is P < 0.0001 by two-way ANOVA with Bonferroni post-hoc test). (I) BAITs improve antigen digestion and uptake of DCs under TGFβ stimulation. DCs were first incubated with <t>Cy5-antigens</t> for 12 h, followed by medium replacement and subsequent treatment with Cy3-antigens or Cy3-BAITs for an additional 6 h. Data are presented as mean ± SD.
Cy5 Se Dye, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Jena Bioscience aminoallyl-dutp-cy5
BAITs enhance antigen uptake and digestion by DCs under TGFβ stimulation. (A) Schematic illustration of real-time DC migration assay. BAITs in the lower chamber create a chemokine gradient to attract DCs from the upper chamber. (B) Kinetics of DC migration measured as cell index (n = 3; n.s. is P > 0.05, ∗∗∗∗ is P < 0.0001 by two-way ANOVA with Bonferroni post-hoc test). (C) Crystal violet staining of non-migrated DCs (upper chamber) and Calcein-AM staining of migrated DCs (lower chamber) showing enhanced DC recruitment by BAITs. (D) The antigen uptake efficiency of DCs under varying antigen concentrations with or without TGFβ (n = 5; ∗∗∗ is P < 0.001, ∗∗∗∗ is P < 0.0001 by two-way ANOVA with Bonferroni post-hoc test). (E) Heatmap of immune-related genes in DCs showing upregulation of antigen presentation and co-stimulation markers and downregulation of suppressive factors as antigen concentration increases. (F) Antigen digestion capacity of DCs assessed in the presence or absence of TGFβ (n = 8; ∗∗∗∗ is P < 0.0001 by two-tailed Student's t -test). (G) Fluorescent images showing enhanced antigen uptake in DCs mediated by BAITs (quantified on right; n = 10; ∗∗∗∗ is P < 0.0001 by two-way ANOVA with Bonferroni post-hoc test). (H) Flow cytometry analysis of antigen-positive (Cy3 + ) DCs after incubation with free antigen or BAIT (quantified on right; n = 4; ∗∗∗∗ is P < 0.0001 by two-way ANOVA with Bonferroni post-hoc test). (I) BAITs improve antigen digestion and uptake of DCs under TGFβ stimulation. DCs were first incubated with <t>Cy5-antigens</t> for 12 h, followed by medium replacement and subsequent treatment with Cy3-antigens or Cy3-BAITs for an additional 6 h. Data are presented as mean ± SD.
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BAITs enhance antigen uptake and digestion by DCs under TGFβ stimulation. (A) Schematic illustration of real-time DC migration assay. BAITs in the lower chamber create a chemokine gradient to attract DCs from the upper chamber. (B) Kinetics of DC migration measured as cell index (n = 3; n.s. is P > 0.05, ∗∗∗∗ is P < 0.0001 by two-way ANOVA with Bonferroni post-hoc test). (C) Crystal violet staining of non-migrated DCs (upper chamber) and Calcein-AM staining of migrated DCs (lower chamber) showing enhanced DC recruitment by BAITs. (D) The antigen uptake efficiency of DCs under varying antigen concentrations with or without TGFβ (n = 5; ∗∗∗ is P < 0.001, ∗∗∗∗ is P < 0.0001 by two-way ANOVA with Bonferroni post-hoc test). (E) Heatmap of immune-related genes in DCs showing upregulation of antigen presentation and co-stimulation markers and downregulation of suppressive factors as antigen concentration increases. (F) Antigen digestion capacity of DCs assessed in the presence or absence of TGFβ (n = 8; ∗∗∗∗ is P < 0.0001 by two-tailed Student's t -test). (G) Fluorescent images showing enhanced antigen uptake in DCs mediated by BAITs (quantified on right; n = 10; ∗∗∗∗ is P < 0.0001 by two-way ANOVA with Bonferroni post-hoc test). (H) Flow cytometry analysis of antigen-positive (Cy3 + ) DCs after incubation with free antigen or BAIT (quantified on right; n = 4; ∗∗∗∗ is P < 0.0001 by two-way ANOVA with Bonferroni post-hoc test). (I) BAITs improve antigen digestion and uptake of DCs under TGFβ stimulation. DCs were first incubated with <t>Cy5-antigens</t> for 12 h, followed by medium replacement and subsequent treatment with Cy3-antigens or Cy3-BAITs for an additional 6 h. Data are presented as mean ± SD.
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BAITs enhance antigen uptake and digestion by DCs under TGFβ stimulation. (A) Schematic illustration of real-time DC migration assay. BAITs in the lower chamber create a chemokine gradient to attract DCs from the upper chamber. (B) Kinetics of DC migration measured as cell index (n = 3; n.s. is P > 0.05, ∗∗∗∗ is P < 0.0001 by two-way ANOVA with Bonferroni post-hoc test). (C) Crystal violet staining of non-migrated DCs (upper chamber) and Calcein-AM staining of migrated DCs (lower chamber) showing enhanced DC recruitment by BAITs. (D) The antigen uptake efficiency of DCs under varying antigen concentrations with or without TGFβ (n = 5; ∗∗∗ is P < 0.001, ∗∗∗∗ is P < 0.0001 by two-way ANOVA with Bonferroni post-hoc test). (E) Heatmap of immune-related genes in DCs showing upregulation of antigen presentation and co-stimulation markers and downregulation of suppressive factors as antigen concentration increases. (F) Antigen digestion capacity of DCs assessed in the presence or absence of TGFβ (n = 8; ∗∗∗∗ is P < 0.0001 by two-tailed Student's t -test). (G) Fluorescent images showing enhanced antigen uptake in DCs mediated by BAITs (quantified on right; n = 10; ∗∗∗∗ is P < 0.0001 by two-way ANOVA with Bonferroni post-hoc test). (H) Flow cytometry analysis of antigen-positive (Cy3 + ) DCs after incubation with free antigen or BAIT (quantified on right; n = 4; ∗∗∗∗ is P < 0.0001 by two-way ANOVA with Bonferroni post-hoc test). (I) BAITs improve antigen digestion and uptake of DCs under TGFβ stimulation. DCs were first incubated with <t>Cy5-antigens</t> for 12 h, followed by medium replacement and subsequent treatment with Cy3-antigens or Cy3-BAITs for an additional 6 h. Data are presented as mean ± SD.
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BAITs enhance antigen uptake and digestion by DCs under TGFβ stimulation. (A) Schematic illustration of real-time DC migration assay. BAITs in the lower chamber create a chemokine gradient to attract DCs from the upper chamber. (B) Kinetics of DC migration measured as cell index (n = 3; n.s. is P > 0.05, ∗∗∗∗ is P < 0.0001 by two-way ANOVA with Bonferroni post-hoc test). (C) Crystal violet staining of non-migrated DCs (upper chamber) and Calcein-AM staining of migrated DCs (lower chamber) showing enhanced DC recruitment by BAITs. (D) The antigen uptake efficiency of DCs under varying antigen concentrations with or without TGFβ (n = 5; ∗∗∗ is P < 0.001, ∗∗∗∗ is P < 0.0001 by two-way ANOVA with Bonferroni post-hoc test). (E) Heatmap of immune-related genes in DCs showing upregulation of antigen presentation and co-stimulation markers and downregulation of suppressive factors as antigen concentration increases. (F) Antigen digestion capacity of DCs assessed in the presence or absence of TGFβ (n = 8; ∗∗∗∗ is P < 0.0001 by two-tailed Student's t -test). (G) Fluorescent images showing enhanced antigen uptake in DCs mediated by BAITs (quantified on right; n = 10; ∗∗∗∗ is P < 0.0001 by two-way ANOVA with Bonferroni post-hoc test). (H) Flow cytometry analysis of antigen-positive (Cy3 + ) DCs after incubation with free antigen or BAIT (quantified on right; n = 4; ∗∗∗∗ is P < 0.0001 by two-way ANOVA with Bonferroni post-hoc test). (I) BAITs improve antigen digestion and uptake of DCs under TGFβ stimulation. DCs were first incubated with <t>Cy5-antigens</t> for 12 h, followed by medium replacement and subsequent treatment with Cy3-antigens or Cy3-BAITs for an additional 6 h. Data are presented as mean ± SD.
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Image Search Results


In vivo photoacoustic imaging and analysis of the vulnerability of atherosclerotic plaque. ( A - G ) Ex vivo distribution of HMCN@Cy5.5 , Scr-HMCN@Cy5.5 , and OPN-HMCN@Cy5.5 in various organs—specifically the aorta ( B ), heart ( C ), liver ( D ), spleen ( E ), lung ( F ), and kidney ( G )—from apoE −/− mice at 0, 6, 12, and 24 h post-intravenous injection (n = 3). ( H ) Confocal images demonstrate the colocalization of OPN with CY5.5-labeled nanoparticles in aortic roots (n = 6, scale bars, 200 μm). ( I ) Quantitative analysis of the relative MFI of OPN and CY5.5 in different treatment groups. ( J , K ) Photoacoustic images and quantitative analysis of signal intensities of atherosclerotic plaque in carotid arteries of both healthy and atherosclerosis mice (n = 3). For each animal, longitudinal PA imaging was performed on the same carotid artery at predefined anatomical landmarks across different time points. Photoacoustic images were acquired with depth calibration based on acoustic time-of-flight measurements, converting ultrasound echo delay into depth using the predefined sound velocity in soft tissue. A calibrated depth scale bar is shown in each image, with an effective imaging depth of approximately 7 mm. ( L , M ) Pathological staining of atherosclerotic plaques in the carotid artery and aortic arch includes ORO and Masson staining (scale bar = 200 μm), as well as α -SMA, and CD68 fluorescent staining (scale bar = 100 μm each). ( N - Q ) The statistical analysis of ( N ) ORO staining (namely the percentage of LD area), ( O ) Masson staining (namely the percentage of collagen fiber area), ( P ) α -SMA fluorescent staining (namely the percentage of smooth muscle cell area) and ( Q ) CD68 fluorescent staining (namely the percentage of macrophage-derived foam cell area). ( R ) Vulnerability scores of aortic arch and carotid artery plaques. ∗ P < 0.05, ∗∗ P < 0.01, and ∗∗∗∗ P < 0.0001.

Journal: Bioactive Materials

Article Title: A foam cell-targeted lipophagy restoration strategy stabilizes vulnerable atherosclerotic plaques

doi: 10.1016/j.bioactmat.2026.02.041

Figure Lengend Snippet: In vivo photoacoustic imaging and analysis of the vulnerability of atherosclerotic plaque. ( A - G ) Ex vivo distribution of HMCN@Cy5.5 , Scr-HMCN@Cy5.5 , and OPN-HMCN@Cy5.5 in various organs—specifically the aorta ( B ), heart ( C ), liver ( D ), spleen ( E ), lung ( F ), and kidney ( G )—from apoE −/− mice at 0, 6, 12, and 24 h post-intravenous injection (n = 3). ( H ) Confocal images demonstrate the colocalization of OPN with CY5.5-labeled nanoparticles in aortic roots (n = 6, scale bars, 200 μm). ( I ) Quantitative analysis of the relative MFI of OPN and CY5.5 in different treatment groups. ( J , K ) Photoacoustic images and quantitative analysis of signal intensities of atherosclerotic plaque in carotid arteries of both healthy and atherosclerosis mice (n = 3). For each animal, longitudinal PA imaging was performed on the same carotid artery at predefined anatomical landmarks across different time points. Photoacoustic images were acquired with depth calibration based on acoustic time-of-flight measurements, converting ultrasound echo delay into depth using the predefined sound velocity in soft tissue. A calibrated depth scale bar is shown in each image, with an effective imaging depth of approximately 7 mm. ( L , M ) Pathological staining of atherosclerotic plaques in the carotid artery and aortic arch includes ORO and Masson staining (scale bar = 200 μm), as well as α -SMA, and CD68 fluorescent staining (scale bar = 100 μm each). ( N - Q ) The statistical analysis of ( N ) ORO staining (namely the percentage of LD area), ( O ) Masson staining (namely the percentage of collagen fiber area), ( P ) α -SMA fluorescent staining (namely the percentage of smooth muscle cell area) and ( Q ) CD68 fluorescent staining (namely the percentage of macrophage-derived foam cell area). ( R ) Vulnerability scores of aortic arch and carotid artery plaques. ∗ P < 0.05, ∗∗ P < 0.01, and ∗∗∗∗ P < 0.0001.

Article Snippet: PEG-NH2 and Cy5.5 were obtained from MedChemExpress, Shanghai, China.

Techniques: In Vivo, Imaging, Ex Vivo, Injection, Labeling, Staining, Derivative Assay

BAITs enhance antigen uptake and digestion by DCs under TGFβ stimulation. (A) Schematic illustration of real-time DC migration assay. BAITs in the lower chamber create a chemokine gradient to attract DCs from the upper chamber. (B) Kinetics of DC migration measured as cell index (n = 3; n.s. is P > 0.05, ∗∗∗∗ is P < 0.0001 by two-way ANOVA with Bonferroni post-hoc test). (C) Crystal violet staining of non-migrated DCs (upper chamber) and Calcein-AM staining of migrated DCs (lower chamber) showing enhanced DC recruitment by BAITs. (D) The antigen uptake efficiency of DCs under varying antigen concentrations with or without TGFβ (n = 5; ∗∗∗ is P < 0.001, ∗∗∗∗ is P < 0.0001 by two-way ANOVA with Bonferroni post-hoc test). (E) Heatmap of immune-related genes in DCs showing upregulation of antigen presentation and co-stimulation markers and downregulation of suppressive factors as antigen concentration increases. (F) Antigen digestion capacity of DCs assessed in the presence or absence of TGFβ (n = 8; ∗∗∗∗ is P < 0.0001 by two-tailed Student's t -test). (G) Fluorescent images showing enhanced antigen uptake in DCs mediated by BAITs (quantified on right; n = 10; ∗∗∗∗ is P < 0.0001 by two-way ANOVA with Bonferroni post-hoc test). (H) Flow cytometry analysis of antigen-positive (Cy3 + ) DCs after incubation with free antigen or BAIT (quantified on right; n = 4; ∗∗∗∗ is P < 0.0001 by two-way ANOVA with Bonferroni post-hoc test). (I) BAITs improve antigen digestion and uptake of DCs under TGFβ stimulation. DCs were first incubated with Cy5-antigens for 12 h, followed by medium replacement and subsequent treatment with Cy3-antigens or Cy3-BAITs for an additional 6 h. Data are presented as mean ± SD.

Journal: Bioactive Materials

Article Title: Countering postoperative immune suppression with a self-assembling dendritic cell nanovaccine

doi: 10.1016/j.bioactmat.2026.05.005

Figure Lengend Snippet: BAITs enhance antigen uptake and digestion by DCs under TGFβ stimulation. (A) Schematic illustration of real-time DC migration assay. BAITs in the lower chamber create a chemokine gradient to attract DCs from the upper chamber. (B) Kinetics of DC migration measured as cell index (n = 3; n.s. is P > 0.05, ∗∗∗∗ is P < 0.0001 by two-way ANOVA with Bonferroni post-hoc test). (C) Crystal violet staining of non-migrated DCs (upper chamber) and Calcein-AM staining of migrated DCs (lower chamber) showing enhanced DC recruitment by BAITs. (D) The antigen uptake efficiency of DCs under varying antigen concentrations with or without TGFβ (n = 5; ∗∗∗ is P < 0.001, ∗∗∗∗ is P < 0.0001 by two-way ANOVA with Bonferroni post-hoc test). (E) Heatmap of immune-related genes in DCs showing upregulation of antigen presentation and co-stimulation markers and downregulation of suppressive factors as antigen concentration increases. (F) Antigen digestion capacity of DCs assessed in the presence or absence of TGFβ (n = 8; ∗∗∗∗ is P < 0.0001 by two-tailed Student's t -test). (G) Fluorescent images showing enhanced antigen uptake in DCs mediated by BAITs (quantified on right; n = 10; ∗∗∗∗ is P < 0.0001 by two-way ANOVA with Bonferroni post-hoc test). (H) Flow cytometry analysis of antigen-positive (Cy3 + ) DCs after incubation with free antigen or BAIT (quantified on right; n = 4; ∗∗∗∗ is P < 0.0001 by two-way ANOVA with Bonferroni post-hoc test). (I) BAITs improve antigen digestion and uptake of DCs under TGFβ stimulation. DCs were first incubated with Cy5-antigens for 12 h, followed by medium replacement and subsequent treatment with Cy3-antigens or Cy3-BAITs for an additional 6 h. Data are presented as mean ± SD.

Article Snippet: For MHC I analysis, the cells were incubated with rat CoraLite Plus 488 anti-mouse LAMP1 antibody (1:200) and rabbit anti-mouse MHC I antibody (1:100) overnight at 4 °C, followed by Cy5-conjugated anti-rabbit secondary antibody (1:200) for 1 h at 37 °C.

Techniques: Migration, Staining, Immunopeptidomics, Concentration Assay, Two Tailed Test, Flow Cytometry, Incubation