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Exosome Diagnostics cd73

Adenosine production and receptor-mediated effects in inflammatory and hypoxic microenvironments. This schematic illustrates the dual pathways of adenosine generation and its downstream immunoregulatory and fibrotic effects in AS. Under conditions of cellular stress—including inflammation, hypoxia, tissue damage, or immune activation—extracellular ATP is released and sequentially hydrolyzed by the ectonucleotidases CD39 and <t>CD73</t> into adenosine at the cell surface. In parallel, stress-induced exosome release contributes to localized adenosine production by delivering CD73, ATP/ADP substrates, and regulatory microRNAs; these vesicles act as mobile enzymatic platforms, amplifying adenosine synthesis in inflamed niches. The resulting adenosine engages four G protein–coupled receptors (A1, A2A, A2B, A3), each with distinct affinities and cell-specific effects. The accompanying table summarizes receptor-mediated outcomes across key immune and stromal cell types: A2A receptor activation promotes FOXP3 + Treg function, suppresses Th17 differentiation, and skews macrophages toward an anti-inflammatory M2 phenotype. In contrast, A2B receptor signaling—preferentially activated at higher adenosine concentrations—enhances fibroblast activation, promotes IL-6 and TNF-α production, and drives fibrotic remodeling and angiogenesis in stromal niches. A1 and A3 receptors can exert additional anti-inflammatory influences in specific contexts, including effects on neutrophils and antigen-presenting cells. Together, this figure highlights the spatial and functional complexity of adenosine signaling in AS and the rationale for receptor-selective and exosome-enabled strategies, “not directly established in AS” = effect reported in related systems but not yet shown directly in axial spondyloarthritis, † = context-dependent effect; outcome can vary with cell type, adenosine level, tissue environment, or disease stage.

Cd73, supplied by Exosome Diagnostics, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "Restoring adenosine balance in axial spondyloarthritis: a stage-specific framework for immune and structural modulation"

Article Title: Restoring adenosine balance in axial spondyloarthritis: a stage-specific framework for immune and structural modulation

Journal: Frontiers in Immunology

doi: 10.3389/fimmu.2026.1738120

Figure Legend Snippet: Adenosine production and receptor-mediated effects in inflammatory and hypoxic microenvironments. This schematic illustrates the dual pathways of adenosine generation and its downstream immunoregulatory and fibrotic effects in AS. Under conditions of cellular stress—including inflammation, hypoxia, tissue damage, or immune activation—extracellular ATP is released and sequentially hydrolyzed by the ectonucleotidases CD39 and CD73 into adenosine at the cell surface. In parallel, stress-induced exosome release contributes to localized adenosine production by delivering CD73, ATP/ADP substrates, and regulatory microRNAs; these vesicles act as mobile enzymatic platforms, amplifying adenosine synthesis in inflamed niches. The resulting adenosine engages four G protein–coupled receptors (A1, A2A, A2B, A3), each with distinct affinities and cell-specific effects. The accompanying table summarizes receptor-mediated outcomes across key immune and stromal cell types: A2A receptor activation promotes FOXP3 + Treg function, suppresses Th17 differentiation, and skews macrophages toward an anti-inflammatory M2 phenotype. In contrast, A2B receptor signaling—preferentially activated at higher adenosine concentrations—enhances fibroblast activation, promotes IL-6 and TNF-α production, and drives fibrotic remodeling and angiogenesis in stromal niches. A1 and A3 receptors can exert additional anti-inflammatory influences in specific contexts, including effects on neutrophils and antigen-presenting cells. Together, this figure highlights the spatial and functional complexity of adenosine signaling in AS and the rationale for receptor-selective and exosome-enabled strategies, “not directly established in AS” = effect reported in related systems but not yet shown directly in axial spondyloarthritis, † = context-dependent effect; outcome can vary with cell type, adenosine level, tissue environment, or disease stage.

Techniques Used: Activation Assay, Functional Assay

Integrated mechanisms of immune dysregulation, genetic predisposition, and adenosine-mediated modulation in AS. This composite figure illustrates the multifaceted pathogenesis of AS, integrating immune–stromal crosstalk, genetic drivers, cytokine signaling, and purinergic regulation. (1) Cellular interactions in enthesitis: Mechanical stress and microdamage at the enthesis activate macrophages and dendritic cells, which secrete IL-23, IL-6, and TNF-α. These cytokines promote Th17 cell expansion and IL-17/IL-22 production, which in turn activate fibroblasts. Activated fibroblasts release RANKL and pro-osteogenic mediators, driving osteoclastogenesis and initiating bone resorption. (2) Genetic dysregulation in AS: Misfolding of HLA-B27 in antigen-presenting cells induces endoplasmic reticulum (ER) stress, triggering IL-23 production and perpetuating Th17-driven inflammation. This genetic predisposition reinforces the chronic inflammatory loop at the enthesis. (3) Cytokine-driven bone remodeling: Persistent IL-17, IL-6, and TNF-α signaling promotes osteoclast differentiation and activity, while fibroblast-derived TGF-β and Wnt/BMP pathway activation stimulate osteoblasts and osteoprogenitor cells, leading to pathological new bone formation. (4) Exosome-mediated adenosine modulation: In healthy conditions, exosomes enriched with CD39 and CD73 catalyze the conversion of extracellular ATP to adenosine, which suppresses inflammation via A2A receptor activation on immune cells. In AS, reduced CD39/CD73 expression and elevated ADA/CD26 activity impair adenosine availability, weakening immunosuppressive signaling and allowing unchecked inflammation and stromal activation. Together, these interconnected pathways establish a self-reinforcing cycle of immune dysregulation, stromal remodeling, and ossification, highlighting multiple therapeutic entry points—including exosome-based adenosine restoration and receptor-selective modulation.

Figure Legend Snippet: Integrated mechanisms of immune dysregulation, genetic predisposition, and adenosine-mediated modulation in AS. This composite figure illustrates the multifaceted pathogenesis of AS, integrating immune–stromal crosstalk, genetic drivers, cytokine signaling, and purinergic regulation. (1) Cellular interactions in enthesitis: Mechanical stress and microdamage at the enthesis activate macrophages and dendritic cells, which secrete IL-23, IL-6, and TNF-α. These cytokines promote Th17 cell expansion and IL-17/IL-22 production, which in turn activate fibroblasts. Activated fibroblasts release RANKL and pro-osteogenic mediators, driving osteoclastogenesis and initiating bone resorption. (2) Genetic dysregulation in AS: Misfolding of HLA-B27 in antigen-presenting cells induces endoplasmic reticulum (ER) stress, triggering IL-23 production and perpetuating Th17-driven inflammation. This genetic predisposition reinforces the chronic inflammatory loop at the enthesis. (3) Cytokine-driven bone remodeling: Persistent IL-17, IL-6, and TNF-α signaling promotes osteoclast differentiation and activity, while fibroblast-derived TGF-β and Wnt/BMP pathway activation stimulate osteoblasts and osteoprogenitor cells, leading to pathological new bone formation. (4) Exosome-mediated adenosine modulation: In healthy conditions, exosomes enriched with CD39 and CD73 catalyze the conversion of extracellular ATP to adenosine, which suppresses inflammation via A2A receptor activation on immune cells. In AS, reduced CD39/CD73 expression and elevated ADA/CD26 activity impair adenosine availability, weakening immunosuppressive signaling and allowing unchecked inflammation and stromal activation. Together, these interconnected pathways establish a self-reinforcing cycle of immune dysregulation, stromal remodeling, and ossification, highlighting multiple therapeutic entry points—including exosome-based adenosine restoration and receptor-selective modulation.

Techniques Used: Activity Assay, Derivative Assay, Activation Assay, Expressing

Mechanistic divergence explaining methotrexate (MTX) ineffectiveness in AS compared to RA. This comparative schematic illustrates a potential mechanism for MTX’s limited effect in AS but effective in RA and should be interpreted as a hypothesis pending AS−specific validation. Left panel (RA): MTX inhibits AICAR transformylase, leading to intracellular accumulation of AICAR, which inhibits ADA. This results in increased extracellular adenosine levels. Concurrently, CD39 and CD73 ectonucleotidases efficiently convert extracellular ATP to adenosine. The accumulated adenosine activates high-affinity A2A receptors on immune cells, suppressing NF-κB and STAT3 signaling pathways and reducing pro-inflammatory cytokines (IL-6, TNF-α, IL-17). This cascade promotes immune tolerance and clinical remission. Right panel (AS): Although MTX similarly increases AICAR, the downstream adenosine pathway is disrupted. CD39 and CD73 expression is reduced on immune cells, impairing adenosine synthesis. Simultaneously, ADA and its surface anchor CD26 are upregulated on Th17 cells and fibroblasts, accelerating adenosine degradation. As a result, extracellular adenosine remains insufficient to activate A2A receptors. Instead, localized adenosine accumulation in stromal niches engages low-affinity A2B receptors on fibroblasts and osteoprogenitors, triggering Smad3 and STAT3 signaling. This promotes collagen synthesis, connective tissue growth factor (CTGF) expression, and pathological bone formation. Thus, MTX frequently fails to suppress inflammation and may inadvertently contribute to fibrotic remodeling in AS. This figure encapsulates the concept of purinergic resistance in AS and underscores the need for stage-specific, receptor-selective, and compartment-aware therapeutic strategies that go beyond conventional MTX mechanisms. The AS panel represents a mechanistic hypothesis; the relative contributions of ectonucleotidase deficiency and ADA/CD26-mediated degradation to MTX non-responsiveness remain to be validated in AS.

Figure Legend Snippet: Mechanistic divergence explaining methotrexate (MTX) ineffectiveness in AS compared to RA. This comparative schematic illustrates a potential mechanism for MTX’s limited effect in AS but effective in RA and should be interpreted as a hypothesis pending AS−specific validation. Left panel (RA): MTX inhibits AICAR transformylase, leading to intracellular accumulation of AICAR, which inhibits ADA. This results in increased extracellular adenosine levels. Concurrently, CD39 and CD73 ectonucleotidases efficiently convert extracellular ATP to adenosine. The accumulated adenosine activates high-affinity A2A receptors on immune cells, suppressing NF-κB and STAT3 signaling pathways and reducing pro-inflammatory cytokines (IL-6, TNF-α, IL-17). This cascade promotes immune tolerance and clinical remission. Right panel (AS): Although MTX similarly increases AICAR, the downstream adenosine pathway is disrupted. CD39 and CD73 expression is reduced on immune cells, impairing adenosine synthesis. Simultaneously, ADA and its surface anchor CD26 are upregulated on Th17 cells and fibroblasts, accelerating adenosine degradation. As a result, extracellular adenosine remains insufficient to activate A2A receptors. Instead, localized adenosine accumulation in stromal niches engages low-affinity A2B receptors on fibroblasts and osteoprogenitors, triggering Smad3 and STAT3 signaling. This promotes collagen synthesis, connective tissue growth factor (CTGF) expression, and pathological bone formation. Thus, MTX frequently fails to suppress inflammation and may inadvertently contribute to fibrotic remodeling in AS. This figure encapsulates the concept of purinergic resistance in AS and underscores the need for stage-specific, receptor-selective, and compartment-aware therapeutic strategies that go beyond conventional MTX mechanisms. The AS panel represents a mechanistic hypothesis; the relative contributions of ectonucleotidase deficiency and ADA/CD26-mediated degradation to MTX non-responsiveness remain to be validated in AS.

Techniques Used: Biomarker Discovery, Protein-Protein interactions, Expressing

Image Search Results

Schematic illustration of the T-score and S-score. The tumor bed was divided into tumor and stromal compartments, and the T-score and S-score represent the quantitative measurements of CD73 (CD3, CD8, Foxp3, and CD163) expression or lymphocyte infiltration within each compartment, respectively.

Journal: Cancers

Article Title: High CD73 Expression Is Associated with Poor Prognosis in Biliary Tract Cancer Through Reduced Stromal Tumor-Infiltrating Lymphocytes

doi: 10.3390/cancers18060975

Figure Lengend Snippet: Schematic illustration of the T-score and S-score. The tumor bed was divided into tumor and stromal compartments, and the T-score and S-score represent the quantitative measurements of CD73 (CD3, CD8, Foxp3, and CD163) expression or lymphocyte infiltration within each compartment, respectively.

Article Snippet: Eligible specimens were subjected to IHC staining using a rabbit monoclonal anti-CD73 antibody (#13160, Cell Signaling Technology, Danvers, MA, USA) diluted 1:100, a rabbit polyclonal anti-CD3 antibody (Dako #IR503, Agilent, Santa Clara, CA, USA), a mouse monoclonal anti-CD8 antibody (Dako #IR623, Agilent, Santa Clara, CA, USA), a mouse monoclonal anti-CD163 antibody (#CD163-L-CE, Leica Biosystems, Nussloch, Germany) diluted 1:500, and a mouse monoclonal anti-Foxp3 antibody (#ab20034, abcam, Cambridge, UK) diluted 1:100.

Techniques: Expressing

Representative IHC staining images ( left ) and corresponding AI-based analysis images generated by DeepPathFinder™ ( right ) for CD73, CD3, CD8, Foxp3, and CD163 (original magnification approximately ×200). IHC-positive areas (cyan) were automatically identified and overlaid onto tumor regions (green) delineated on the corresponding H&E–stained images, enabling quantitative assessment of IHC-positive area within the tumor compartment.

Journal: Cancers

Article Title: High CD73 Expression Is Associated with Poor Prognosis in Biliary Tract Cancer Through Reduced Stromal Tumor-Infiltrating Lymphocytes

doi: 10.3390/cancers18060975

Figure Lengend Snippet: Representative IHC staining images ( left ) and corresponding AI-based analysis images generated by DeepPathFinder™ ( right ) for CD73, CD3, CD8, Foxp3, and CD163 (original magnification approximately ×200). IHC-positive areas (cyan) were automatically identified and overlaid onto tumor regions (green) delineated on the corresponding H&E–stained images, enabling quantitative assessment of IHC-positive area within the tumor compartment.

Techniques: Immunohistochemistry, Generated, Staining

Effect of the CD73 and TIL scores. Kaplan–Meier curves of the overall survival in 100 patients ( a ) 50 in the T-CD73-high group and 50 in the T-CD73-low group ( b ) 50 in the S-CD73-high group and 50 in the S-CD73-low group ( c ) 50 in the T-TIL-high group and 50 in the T-TIL-low group ( d ) 50 in the S-TIL-high group and 50 in the S-TIL-low group.

Journal: Cancers

Article Title: High CD73 Expression Is Associated with Poor Prognosis in Biliary Tract Cancer Through Reduced Stromal Tumor-Infiltrating Lymphocytes

doi: 10.3390/cancers18060975

Figure Lengend Snippet: Effect of the CD73 and TIL scores. Kaplan–Meier curves of the overall survival in 100 patients ( a ) 50 in the T-CD73-high group and 50 in the T-CD73-low group ( b ) 50 in the S-CD73-high group and 50 in the S-CD73-low group ( c ) 50 in the T-TIL-high group and 50 in the T-TIL-low group ( d ) 50 in the S-TIL-high group and 50 in the S-TIL-low group.

Techniques:

Correlations between T-CD73 and TIL scores/immune cell subsets. Spearman’s rank correlation coefficient between ( a ) T-CD73 and T-TIL scores and ( b ) T-CD73 and S-TIL scores.

Journal: Cancers

Article Title: High CD73 Expression Is Associated with Poor Prognosis in Biliary Tract Cancer Through Reduced Stromal Tumor-Infiltrating Lymphocytes

doi: 10.3390/cancers18060975

Figure Lengend Snippet: Correlations between T-CD73 and TIL scores/immune cell subsets. Spearman’s rank correlation coefficient between ( a ) T-CD73 and T-TIL scores and ( b ) T-CD73 and S-TIL scores.

Techniques:

Correlations between T-CD73 and immune cell subsets. Spearman’s rank correlation coefficient between ( a ) T-CD73 and S-CD3 scores and ( b ) T-CD73 and S-CD8 scores.

Journal: Cancers

Article Title: High CD73 Expression Is Associated with Poor Prognosis in Biliary Tract Cancer Through Reduced Stromal Tumor-Infiltrating Lymphocytes

doi: 10.3390/cancers18060975

Figure Lengend Snippet: Correlations between T-CD73 and immune cell subsets. Spearman’s rank correlation coefficient between ( a ) T-CD73 and S-CD3 scores and ( b ) T-CD73 and S-CD8 scores.

Techniques:

Journal: Frontiers in Immunology

Article Title: Restoring adenosine balance in axial spondyloarthritis: a stage-specific framework for immune and structural modulation

doi: 10.3389/fimmu.2026.1738120

Figure Lengend Snippet: Adenosine production and receptor-mediated effects in inflammatory and hypoxic microenvironments. This schematic illustrates the dual pathways of adenosine generation and its downstream immunoregulatory and fibrotic effects in AS. Under conditions of cellular stress—including inflammation, hypoxia, tissue damage, or immune activation—extracellular ATP is released and sequentially hydrolyzed by the ectonucleotidases CD39 and CD73 into adenosine at the cell surface. In parallel, stress-induced exosome release contributes to localized adenosine production by delivering CD73, ATP/ADP substrates, and regulatory microRNAs; these vesicles act as mobile enzymatic platforms, amplifying adenosine synthesis in inflamed niches. The resulting adenosine engages four G protein–coupled receptors (A1, A2A, A2B, A3), each with distinct affinities and cell-specific effects. The accompanying table summarizes receptor-mediated outcomes across key immune and stromal cell types: A2A receptor activation promotes FOXP3 + Treg function, suppresses Th17 differentiation, and skews macrophages toward an anti-inflammatory M2 phenotype. In contrast, A2B receptor signaling—preferentially activated at higher adenosine concentrations—enhances fibroblast activation, promotes IL-6 and TNF-α production, and drives fibrotic remodeling and angiogenesis in stromal niches. A1 and A3 receptors can exert additional anti-inflammatory influences in specific contexts, including effects on neutrophils and antigen-presenting cells. Together, this figure highlights the spatial and functional complexity of adenosine signaling in AS and the rationale for receptor-selective and exosome-enabled strategies, “not directly established in AS” = effect reported in related systems but not yet shown directly in axial spondyloarthritis, † = context-dependent effect; outcome can vary with cell type, adenosine level, tissue environment, or disease stage.

Article Snippet: Exosome-mediated restoration of CD39 and CD73 represents one of the most biologically aligned approaches to re-establishing adenosine balance.

Techniques: Activation Assay, Functional Assay

Journal: Frontiers in Immunology

Article Title: Restoring adenosine balance in axial spondyloarthritis: a stage-specific framework for immune and structural modulation

doi: 10.3389/fimmu.2026.1738120

Figure Lengend Snippet: Integrated mechanisms of immune dysregulation, genetic predisposition, and adenosine-mediated modulation in AS. This composite figure illustrates the multifaceted pathogenesis of AS, integrating immune–stromal crosstalk, genetic drivers, cytokine signaling, and purinergic regulation. (1) Cellular interactions in enthesitis: Mechanical stress and microdamage at the enthesis activate macrophages and dendritic cells, which secrete IL-23, IL-6, and TNF-α. These cytokines promote Th17 cell expansion and IL-17/IL-22 production, which in turn activate fibroblasts. Activated fibroblasts release RANKL and pro-osteogenic mediators, driving osteoclastogenesis and initiating bone resorption. (2) Genetic dysregulation in AS: Misfolding of HLA-B27 in antigen-presenting cells induces endoplasmic reticulum (ER) stress, triggering IL-23 production and perpetuating Th17-driven inflammation. This genetic predisposition reinforces the chronic inflammatory loop at the enthesis. (3) Cytokine-driven bone remodeling: Persistent IL-17, IL-6, and TNF-α signaling promotes osteoclast differentiation and activity, while fibroblast-derived TGF-β and Wnt/BMP pathway activation stimulate osteoblasts and osteoprogenitor cells, leading to pathological new bone formation. (4) Exosome-mediated adenosine modulation: In healthy conditions, exosomes enriched with CD39 and CD73 catalyze the conversion of extracellular ATP to adenosine, which suppresses inflammation via A2A receptor activation on immune cells. In AS, reduced CD39/CD73 expression and elevated ADA/CD26 activity impair adenosine availability, weakening immunosuppressive signaling and allowing unchecked inflammation and stromal activation. Together, these interconnected pathways establish a self-reinforcing cycle of immune dysregulation, stromal remodeling, and ossification, highlighting multiple therapeutic entry points—including exosome-based adenosine restoration and receptor-selective modulation.

Article Snippet: Exosome-mediated restoration of CD39 and CD73 represents one of the most biologically aligned approaches to re-establishing adenosine balance.

Techniques: Activity Assay, Derivative Assay, Activation Assay, Expressing

Journal: Frontiers in Immunology

Article Title: Restoring adenosine balance in axial spondyloarthritis: a stage-specific framework for immune and structural modulation

doi: 10.3389/fimmu.2026.1738120

Figure Lengend Snippet: Mechanistic divergence explaining methotrexate (MTX) ineffectiveness in AS compared to RA. This comparative schematic illustrates a potential mechanism for MTX’s limited effect in AS but effective in RA and should be interpreted as a hypothesis pending AS−specific validation. Left panel (RA): MTX inhibits AICAR transformylase, leading to intracellular accumulation of AICAR, which inhibits ADA. This results in increased extracellular adenosine levels. Concurrently, CD39 and CD73 ectonucleotidases efficiently convert extracellular ATP to adenosine. The accumulated adenosine activates high-affinity A2A receptors on immune cells, suppressing NF-κB and STAT3 signaling pathways and reducing pro-inflammatory cytokines (IL-6, TNF-α, IL-17). This cascade promotes immune tolerance and clinical remission. Right panel (AS): Although MTX similarly increases AICAR, the downstream adenosine pathway is disrupted. CD39 and CD73 expression is reduced on immune cells, impairing adenosine synthesis. Simultaneously, ADA and its surface anchor CD26 are upregulated on Th17 cells and fibroblasts, accelerating adenosine degradation. As a result, extracellular adenosine remains insufficient to activate A2A receptors. Instead, localized adenosine accumulation in stromal niches engages low-affinity A2B receptors on fibroblasts and osteoprogenitors, triggering Smad3 and STAT3 signaling. This promotes collagen synthesis, connective tissue growth factor (CTGF) expression, and pathological bone formation. Thus, MTX frequently fails to suppress inflammation and may inadvertently contribute to fibrotic remodeling in AS. This figure encapsulates the concept of purinergic resistance in AS and underscores the need for stage-specific, receptor-selective, and compartment-aware therapeutic strategies that go beyond conventional MTX mechanisms. The AS panel represents a mechanistic hypothesis; the relative contributions of ectonucleotidase deficiency and ADA/CD26-mediated degradation to MTX non-responsiveness remain to be validated in AS.

Article Snippet: Exosome-mediated restoration of CD39 and CD73 represents one of the most biologically aligned approaches to re-establishing adenosine balance.

Techniques: Biomarker Discovery, Protein-Protein interactions, Expressing

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