immunofluorescence analysis (Cell Signaling Technology Inc)
Cell Signaling Technology Inc is a verified supplier 
Cell Signaling Technology Inc manufactures this product 
86
Structured Review
Cell Signaling Technology Inc
immunofluorescence analysis
Immunofluorescence Analysis, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/immunofluorescence+analysis/pmc12598499-285-7-11
Average 86 stars, based on 1 article reviews
Immunofluorescence Analysis, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/immunofluorescence+analysis/pmc12598499-285-7-11
Average 86 stars, based on 1 article reviews
immunofluorescence analysis - by Bioz Stars,
2026-09
86/100 stars
Images
1) Product Images from "Host Translational Control by Stress Granules Promotes Mycobacterium tuberculosis Pathogenesis"
Article Title: Host Translational Control by Stress Granules Promotes Mycobacterium tuberculosis Pathogenesis
Journal: MedComm
doi: 10.1002/mco2.70479
Figure Legend Snippet: Mtb infection triggers robust SG formation in macrophages. (A) Immunofluorescence of lung tissues from UN and infected mice. G3bp1 fluorescence intensity was visualized in rainbow color to highlight differences in signal intensity. Scale bar indicates 50 µm. (B, C) Quantification of G3bp1 mean fluorescence intensity (MFI) (B) and G3bp1‐positive foci per area (C) from (A). Data are presented as mean ± SEM. **** p < 0.0001. N = 12. (D) Immunoblot of SG‐related proteins in lung lysates of UN and Mtb‐infected mice. (E) Immunofluorescence of SG markers in BMDMs infected with Mtb (MOI 1, 12 hpi). Scale bar indicates 10 µm. (F) Immunoblot of SG proteins in BMDMs at indicated times (MOI 1). (G) Quantification of relative band intensities from (F), normalized to β‐Actin. Data are presented as relative band intensities compared to UN. **** p < 0.0001. N = 3. (H) Immunofluorescence G3bp1 in H37Rv‐GFP infected BMDMs (MOI 1, 12 hpi). White arrowhead indicates H37Rv‐GFP‐negative cells. Scale bar indicates 10 µm. (I) Quantification of G3bp1‐positive cell ratio in H37Rv‐GFP − cells or H37Rv‐GFP + cells from (H). **** p < 0.0001. N = 20.
Techniques Used: Infection, Immunofluorescence, Fluorescence, Western Blot
Figure Legend Snippet: Intracellular ATP level regulates the dynamics of SGs which affect innate immune activity of macrophages. (A) Immunofluorescence analysis of SGs BMDMs treated with 2‐DG or glucose depletion for 24 h. Scale bar indicates 10 µm. (B) Immunofluorescence analysis of SGs in BMDMs infected with Mtb (MOI 1). Scale bar indicates 10 µm. (C) Intracellular ATP concentrations in BMDMs from (A) were plotted with SG‐positive ratio. The ATP concentration (17.5 nmol/mg protein) correlating with 50% of SG‐positive cells is indicated with dotted line and considered as SG‐inducing ATP concentration. (D) Intracellular ATP concentrations of BMDMs from (B) were plotted with SG‐positive ratio. The SG‐inducing ATP concentration (17.5 nmol/mg protein) from (C) is indicated with dotted line. (E) Intracellular ATP concentrations in zymosan, LPS, and PMA‐treated BMDMs. n.s., nonsignificant, * p < 0.05, **** p < 0.0001. N = 3. (F) Intracellular ATP concentrations in Mtb‐infected BMDMs, following cytochalasin D (Cyto D) treatment. n.s., nonsignificant, **** p < 0.0001. N = 3. (G) Immunoblot analysis of SG markers in BMDMs ± Cyto D after Mtb infection (MOI 1, 24 hpi). (H) Intracellular ATP concentrations in BMDMs treated with empty‐liposome or ATPsome before Mtb infection (MOI 1). n.s., nonsignificant, *** p < 0.001, **** p < 0.0001. N = 3. (I) Immunoblot analysis of SG markers in BMDMs treated as in (H). (J) Immunofluorescence analysis of SGs in GFP‐Mtb‐infected BMDMs ± ATPsome. Scale bar indicates 10 µm. (K) Quantification of Mtb area per cell in (J). * p < 0.05. N = 15. (L) Intracellular Mtb survival in BMDMs ± ATPsome. Data from three independent experiments are shown as mean ± SEM. **** p < 0.0001. N = 3. (M) BMDM viability (LDH assay) after ATPsome or liposome treatment ± infection (MOI 1) Relative to 0 hpi control (Liposome). n.s., nonsignificant; compared within the same time point. N = 3. (N, O) ROS (N; N = 3) and nitrite (O; N = 3) production was measured in media of BMDMs (MOI 1, 24 hpi) ± ATPsome. * p < 0.05. (P) Experimental scheme for pre‐ or post‐treatment of ATPsome. (Q) Immunoblot analysis of BMDMs pre‐ or post‐treated with ATPsome as in (P) (MOI 1, 24 hpi). (R) Intracellular Mtb survival in BMDMs pre/post‐ATPsome treatments (MOI 1). Data from three independent experiments are shown as mean ± SEM. n.s., nonsignificant, ** p < 0.01, *** p < 0.001, **** p < 0.0001. N = 9.
Techniques Used: Activity Assay, Immunofluorescence, Infection, Concentration Assay, Western Blot, Lactate Dehydrogenase Assay, Control
Figure Legend Snippet: SGs suppress host protein synthesis to support Mtb survival. (A) GO analysis of 97 proteins with log 2 ratio (24 hpi/12 hpi) < −1.0 from (Figure ); top five GO categories are shown, ranked by p value. (B) Ribopuromycylation assay of de novo protein synthesis in Mtb‐infected BMDMs (MOI 1). * p < 0.05, *** p < 0.001. N = 3. (C) Ribopuromycylation assay in ISRIB‐treated or untreated BMDMs, during Mtb infection (MOI 1). ** p < 0.01, *** p < 0.001. N = 3. (D) Puromycin immunofluorescence in infected BMDMs ± ISRIB (MOI 1, 12 hpi). Puromycin signal intensity was visualized using a rainbow color scale. Scale bar indicates 20 µm. (E) MFI of the puromycin from (D). Data are presented as mean ± SEM. ** p < 0.01. N = 10. (F) SG‐positive BMDM ratio with or without ISRIB (MOI 1, 12 hpi) were plotted as violin plot with median and quartiles. (G) Intracellular survival of Mtb in ISRIB‐treated or untreated BMDMs (MOI 1). Data are presented as mean ± SEM. n.s., nonsignificant, *** p < 0.001, compared within the same time point. N = 9. (H) Cell viability (LDH assay) of ISRIB‐treated or untreated BMDMs (MOI 1). Relative to 0 hpi ISRIB ‐. n.s., nonsignificant; compared within the same time point. N = 5. (I) Immunofluorescence of SGs in WT (siCont.) and G3bp1/2‐dKD (siG3bp1,2) BMDMs (MOI 1, 24 hpi). Scale bar indicates 20 µm. (J) Quantification of SG‐positive cells from (I). Both Eif3η‐ and Rack1‐positive puncta are considered as SGs. **** p < 0.0001, compared to siCont. N = 15. (K) Immunofluorescence of puromycin in WT and SG neg BMDMs (MOI 1, 12 hpi). Rainbow color gradient indicates puromycin signal intensity. Scale bar indicates 20 µm. (L) MFI of puromycin from (K). ** p < 0.01. N = 10. (M) Ribopuromycylation assay in Mtb‐infected SG neg BMDMs (MOI 1, 12 hpi). (N) Relative puromycin intensity from (M), normalized to β‐Actin. *** p < 0.001, **** p < 0.0001. N = 3. (O) Intracellular survival of Mtb in WT and SG neg BMDMs (MOI 1). Data are presented as mean ± SEM. ** p < 0.01, *** p < 0.001. N = 9. (P) Cell viability (LDH assay) of WT and SG neg BMDMs (MOI 1). Relative to 0 hpi siControl (siCont.). n.s., nonsignificant; compared within the same time point. N = 3.
Techniques Used: Infection, Immunofluorescence, Lactate Dehydrogenase Assay
Figure Legend Snippet: SGs sequester mTORC1 and inhibit cap‐dependent translation during infection. (A) Heatmap of TORC1 complex protein abundance in Mtb‐infected BMDMs (GO: 0031931; MGI v6.22). (B) Immunoblots of mTORC1 activity over time in infected BMDMs (MOI 1); bar graphs show phospho/total ratios. N = 3. (C) Immunoblots of cap‐dependent translation‐related proteins in infected BMDMs (MOI 1). (D) Heatmap of Spearman correlation coefficients ( ρ ) for pairwise expression patterns of proteins analyzed in (C). (E) Immunofluorescence showing colocalization of mTOR and Raptor with G3bp1 in infected macrophages (MOI 1, 12 hpi). Scale bar indicates 5 µm. (F) Dual‐color pixel analysis quantifying colocalization of mTORC1 components with G3bp1 from (E). Pearson correlation coefficients ( r ) are shown. (G) Co‐immunoprecipitation of G3bp1 with mTOR and Raptor from infected BMDMs (MOI 1, 24 hpi). (H) PLA showing spatial interaction of mTOR or Raptor with G3bp1 in infected BMDMs (MOI 1, 12 hpi). Scale bar indicates 5 µm. (I) Immunofluorescence of Astrin colocalizing with G3bp1 and Raptor in infected BMDMs (MOI 1, 12 hpi). Scale bar indicates 4 µm. (J) Immunoblot of Astrin expression in infected BMDMs (MOI 1). (K) PLA showing Astrin interactions with G3bp1 and Raptor in infected BMDMs (MOI 1, 12 hpi). Scale bar indicates 5 µm. (L) Immunoblots of SG markers, mTORC1, cap‐dependent translation proteins, and puromycin incorporation in SG neg BMDMs (MOI 1, 12 hpi).
Techniques Used: Infection, Quantitative Proteomics, Western Blot, Activity Assay, Expressing, Immunofluorescence, Immunoprecipitation
Figure Legend Snippet: SGs impair mitochondrial complex I activity during Mtb infection. (A) Scheme illustrating the breakdown of oxygen consumption following the addition of the specified inhibitors for assessing oxygen consumption rates (OCRs). (B) OCRs in WT and SG neg macrophages infected with Mtb (MOI 1). Cells were transfected with either siControl (left) or siG3bp1/2 (right) for 48 h before infection. (C–E) Quantification of relative basal (C), maximal (D), and ATP‐linked respirations (E) from (B). Normalized to each UN control (pink‐colored dotted line). Pink p value versus UN, black p value versus siCont. n.s., nonsignificant, * p < 0.05, ** p < 0.01. N = 3. (F) Mitochondrial membrane potential (JC‐1 red/green ratio) in infected WT and SG neg BMDMs (MOI 1; normalized to UN; pink dotted line). n.s., nonsignificant, **** p < 0.0001. N = 3. (G) Intracellular ATP concentrations in infected WT and SG neg BMDMs (MOI 1). **** p < 0.0001. N = 3. (H) Lactate secretion from UN or Mtb‐infected WT and SG neg BMDMs (MOI 1). n.s., nonsignificant, * p < 0.05, ** p < 0.01. N = 3. (I) STRING analysis (v11.5) of 37 proteins upregulated in SG neg BMDMs and simultaneously present in the SG proteome, grouped into translation (Cluster 1), mitochondria (Cluster 2), and nuclear import complex (Cluster 3). (J) Immunoblot of whole‐cell lysate (WCL), cytosolic fraction, and mitochondria fraction from Mtb‐infected WT and SG neg BMDMs (MOI 1, 12 hpi). (K) Immunofluorescence analysis of G3bp1‐Ndufa12 colocalization in Mtb‐infected WT and SG neg BMDMs (MOI 1, 12 hpi); line profiles show fluorescence intensity (white arrow). Scale bar indicates 5 µm. (L) Mitochondrial complex I activity in Mtb‐infected WT and SG neg BMDMs (MOI 1, 12 hpi); rotenone as positive control. Relative mitochondrial complex I activity is plotted, compared to uninfected siControl cells. n.s., nonsignificant, **** p < 0.0001. N = 3.
Techniques Used: Activity Assay, Infection, Transfection, Control, Membrane, Western Blot, Immunofluorescence, Fluorescence, Positive Control
Figure Legend Snippet: Inhibition of SGs restores macrophage immune function and restricts Mtb in vivo. (A) Experimental scheme for the in vivo experiments. Mice were transfected with siRNAs via intravenous (i.v.) injection, followed by intratracheal infection with Mtb for 7 days. Seven days postinfection, siRNA transfection was repeated, and the mice were sacrificed another 7 days later for experiments. (B) Immunofluorescence analysis of lung tissues from siRNA‐transfected uninfected (UN) or Mtb‐infected mice. G3bp1 fluorescence intensity was visualized in rainbow color. Scale bar indicates 20 µm. (C) Mean fluorescence intensity (MFI) of G3bp1 signals from (B). * p < 0.05. N = 10. (D) Immunoblot analysis of SG markers, mTORC1, and cap‐dependent translation proteins in lung lysates. (E) Quantification of relative band intensities from (D). Data are presented as relative band intensities compared to uninfected siControl group (UN/siCont.). * p < 0.05, *** p < 0.001. N = 3. (F) H&E staining of lung tissues from siRNA‐transfected uninfected (UN) or Mtb‐infected mice. Scale bar indicates 200 µm. (G) Quantification of TNF and MCP‐1 levels in mouse serum. Data are presented as mean ± SEM. N = 5. (H) Lung CFU in Mtb‐infected mouse lung tissues. Data are presented as mean ± SEM. **** p < 0.0001. N = 7. (I) Immunofluorescence analysis of lung tissues from ISRIB‐treated and Mtb‐infected mice. G3bp1 fluorescence intensity was visualized in rainbow color. Scale bar indicates 10 µm. (J) MFI of G3bp1 from (H). **** p < 0.0001. N = 10. (K) Lung CFU in ISRIB‐treated and Mtb‐infected mouse lung tissues. Data are presented as mean ± SEM. * p < 0.05. N = 9.
Techniques Used: Inhibition, In Vivo, Transfection, Injection, Infection, Immunofluorescence, Fluorescence, Western Blot, Staining
Related Articles
Immunofluorescence:Article Title: Axial Nephron Fate Switching Demonstrates a Plastic System Tunable on Demand Article Snippet: Paraffin sections were dewaxed with the following solution series: 100% Xylene (Sigma-Aldrich) for 10 minutes (2x), 100% ethanol for 1 minutes, 95% ethanol for 1 minute, 80% ethanol for 1 minute, 60% ethanol for 1 minute, 30% ethanol for 1 minute and 2x rinse in deionized water. .. Antigen retrieval was performed as described in the “ Article Title: NaHS alters synaptic plasticity proteins and enhances dendritic arborization to improve cognitive and motor deficits after traumatic brain injury in mice. Article Snippet: Funding information University Grant Commission, Grant/Award Number: F.30-431/2018(BSR) Abstract Background and Purpose: Traumatic brain injury (TBI) is a complex medical condition affecting people globally.. Hydrogen sulfide (H2S) is a recently discovered gaseous mediator and is dysregulated in the brain after TBI.. Sodium hydrogen sulfide (NaHS), a known donor of H2S, is beneficial in various biological processes involving aging and diseases, including injury. Article Title: Pyroptosis‐Inducing Self‐Adaptor to Potentiate Immune Checkpoint Blockade Therapy for Breast Cancer by Reeducating the Treatment‐Recruited Macrophages Article Snippet: Treatment-induced cell pyroptosis can improve the immunogenicity of breast cancer and enhance the efficacy of immune checkpoint blockade (ICB), but the resultant recruitment of immunosuppressive cells impedes the systemic anti-tumor immunity.. Herein, a rationally designed self-adaptor (R@L-MRS17) is developed to initiate breast cancer cell pyroptosis and concomitantly reeducate the pyroptosis-recruited macrophages to enhance the ICB therapy.. Of which, R@L-MRS17 promotes breast cancer-specific drug delivery through CD47 recognition, and enables the plasma membrane targeted photosensitizer insertion through hydrophobic and electrostatic interactions. Article Title: RNF4 and USP7 coordinate spatial regulation of SLX4 stability within the PML nuclear bodies Article Snippet: For western blot analysis, rabbit anti-XPF (A301-315A, 1:1000), rabbit anti-USP7 (A300-033A, 1:1000) from Bethyl; mouse anti-GFP (sc-9996, 1:1000), mouse anti-MUS81 (sc-5332, 1:1000), mouse anti-Ubiquitin (P4D1) (sc-8017, 1:1000), rabbit anti-glyceraldehyde-3-phosphate dehydrogenase (GAPDH; sc-25778, 1:2000), mouse anti-GAPDH (sc-47724, 1:2000), mouse anti-actinin (sc-17829, 1:2000), mouse anti-c-Myc (sc-40, 1:1000), mouse anti-EFP(TRIM25)(E-4) (sc-166926, 1:1000), mouse anti-ERCC1 (sc-17809, 1:1000) from Santa Cruz Biotechnology; mouse anti-HA (MMS-101R, 1:1000) from BioLegend; mouse anti-SLX4 (ab169114, 1:500) from Abcam; mouse anti-RNF4 (H00006047-A01, 1:1000) from Abnova; mouse anti-phospho-Histone H2A.X(ser139) (JBW301, 1:500) from EMD Millipore; rabbit anti-BTBD12 (NBP-2879, 1:500) from Novus; mouse anti-IgG (H + L) (115-035-003, 1:2500), rabbit anti-IgG (H + L) (115-035-003, 1:2500), mouse anti-IgG Light chain (115-035-174, 1:2500), and rabbit anti-IgG Light chain (211-032-171, 1:2500) from Jackson ImmunoResearch. .. Antibodies for Article Title: Axial nephron fate switching demonstrates a plastic system tunable on demand Article Snippet: Paraffin sections were dewaxed with the following solution series: 100% Xylene (Sigma-Aldrich, 247642) for 10 min (2x), 100% ethanol for 1 min, 95% ethanol for 1 min, 80% ethanol for 1 min, 60% ethanol for 1 min, 30% ethanol for 1 min, and 2x rinse in deionized water. .. Antigen retrieval was performed as described in the Article Title: Anti-miR-141-3p maintains homeostasis between autophagy and apoptosis by targeting Yy1 in the fetal lumbosacral defecation center of rats Article Snippet: .. The primary antibody used for Article Title: Host Translational Control by Stress Granules Promotes Mycobacterium tuberculosis Pathogenesis Article Snippet: The following primary antibodies were used for immunoblot analysis: mouse anti‐Eif3η (SCT, sc‐137214), mouse anti‐G3bp1 (SCT, sc‐365338), mouse anti‐Lamp1 (SCT, sc‐20011), mouse anti‐Mfn1 (Invitrogen, MA5‐24789), mouse anti‐mTOR (CST, 4517), mouse anti‐Pabp1 (SCT, sc‐166381), mouse anti‐Raptor (SCT, sc‐81537), mouse anti‐Tomm20 (Sigma, WH0009804M1), rabbit anti‐4E‐BP1 (CST, 9644), rabbit anti‐4E‐BP1‐pT37/46 (CST, 2855), rabbit anti‐β‐Actin (CST, 4970), rabbit anti‐Drp1 (CST, 8570), rabbit anti‐Eif2α (CST, 5324), rabbit anti‐Eif2α‐pS51 (CST, 3597), rabbit anti‐Eif4e (CST, 2067), rabbit anti‐G3bp1 (CST, 61559), rabbit anti‐mTOR‐pS2448 (CST, 5536), rabbit anti‐Ndufa12 (abcam, ab192617), rabbit anti‐Opa1 (CST, 80471), rabbit anti‐p70 S6 Kinase (CST, 2708), rabbit anti‐p70 S6 Kinase‐p389 (CST, 9234), rabbit anti‐SQSTM1/p62 (CST, 23214), rabbit anti‐TSC2 (CST, 4308), rabbit anti‐Astrin (Proteintech, 14726‐1‐AP), rabbit anti‐CoxIV (abcam, ab16056), rabbit anti‐Eif4b (CST, 3592), rabbit anti‐Eif4b‐pS406 (CST, 5399), rabbit anti‐G3bp2 (CST, 31799), rabbit anti‐LC3 (MBL, PM036), rabbit anti‐Parkin (CST, 2132), rabbit anti‐Rack1 (abcam, ab62735), and rabbit anti‐TSC1 (Thermo, PA5‐20131). .. The following primary antibodies were used for Article Title: Aldehyde dehydrogenase 2 attenuates renal injury through inhibiting CYP4A expression. Article Snippet: Renal ischemia-reperfusion injury (IRI) is a prevalent clinical syndrome, yet its underlying pathogenesis remains largely unknown.. Aldehyde dehydrogenase 2 (ALDH2), an enzyme responsible for detoxifying lipid aldehydes, has been suggested to play a protective role against IRI.. In our study, we observed that Aldh2 knock-out C57BL/6 mice experienced more severe renal functional impairment following IRI. Incubation:Article Title: Axial Nephron Fate Switching Demonstrates a Plastic System Tunable on Demand Article Snippet: Paraffin sections were dewaxed with the following solution series: 100% Xylene (Sigma-Aldrich) for 10 minutes (2x), 100% ethanol for 1 minutes, 95% ethanol for 1 minute, 80% ethanol for 1 minute, 60% ethanol for 1 minute, 30% ethanol for 1 minute and 2x rinse in deionized water. .. Antigen retrieval was performed as described in the “ Article Title: Axial nephron fate switching demonstrates a plastic system tunable on demand Article Snippet: Paraffin sections were dewaxed with the following solution series: 100% Xylene (Sigma-Aldrich, 247642) for 10 min (2x), 100% ethanol for 1 min, 95% ethanol for 1 min, 80% ethanol for 1 min, 60% ethanol for 1 min, 30% ethanol for 1 min, and 2x rinse in deionized water. .. Antigen retrieval was performed as described in the Blocking Assay:Article Title: Axial Nephron Fate Switching Demonstrates a Plastic System Tunable on Demand Article Snippet: Paraffin sections were dewaxed with the following solution series: 100% Xylene (Sigma-Aldrich) for 10 minutes (2x), 100% ethanol for 1 minutes, 95% ethanol for 1 minute, 80% ethanol for 1 minute, 60% ethanol for 1 minute, 30% ethanol for 1 minute and 2x rinse in deionized water. .. Antigen retrieval was performed as described in the “ Article Title: Axial nephron fate switching demonstrates a plastic system tunable on demand Article Snippet: Paraffin sections were dewaxed with the following solution series: 100% Xylene (Sigma-Aldrich, 247642) for 10 min (2x), 100% ethanol for 1 min, 95% ethanol for 1 min, 80% ethanol for 1 min, 60% ethanol for 1 min, 30% ethanol for 1 min, and 2x rinse in deionized water. .. Antigen retrieval was performed as described in the Staining:Article Title: NaHS alters synaptic plasticity proteins and enhances dendritic arborization to improve cognitive and motor deficits after traumatic brain injury in mice. Article Snippet: Funding information University Grant Commission, Grant/Award Number: F.30-431/2018(BSR) Abstract Background and Purpose: Traumatic brain injury (TBI) is a complex medical condition affecting people globally.. Hydrogen sulfide (H2S) is a recently discovered gaseous mediator and is dysregulated in the brain after TBI.. Sodium hydrogen sulfide (NaHS), a known donor of H2S, is beneficial in various biological processes involving aging and diseases, including injury. Article Title: Aldehyde dehydrogenase 2 attenuates renal injury through inhibiting CYP4A expression. Article Snippet: Renal ischemia-reperfusion injury (IRI) is a prevalent clinical syndrome, yet its underlying pathogenesis remains largely unknown.. Aldehyde dehydrogenase 2 (ALDH2), an enzyme responsible for detoxifying lipid aldehydes, has been suggested to play a protective role against IRI.. In our study, we observed that Aldh2 knock-out C57BL/6 mice experienced more severe renal functional impairment following IRI. Western Blot:Article Title: Pyroptosis‐Inducing Self‐Adaptor to Potentiate Immune Checkpoint Blockade Therapy for Breast Cancer by Reeducating the Treatment‐Recruited Macrophages Article Snippet: Treatment-induced cell pyroptosis can improve the immunogenicity of breast cancer and enhance the efficacy of immune checkpoint blockade (ICB), but the resultant recruitment of immunosuppressive cells impedes the systemic anti-tumor immunity.. Herein, a rationally designed self-adaptor (R@L-MRS17) is developed to initiate breast cancer cell pyroptosis and concomitantly reeducate the pyroptosis-recruited macrophages to enhance the ICB therapy.. Of which, R@L-MRS17 promotes breast cancer-specific drug delivery through CD47 recognition, and enables the plasma membrane targeted photosensitizer insertion through hydrophobic and electrostatic interactions. |
