galectin 9 tim3 Search Results


t cell function  (Galectin Therapeutics)
86
Galectin Therapeutics t cell function
T Cell Function, supplied by Galectin Therapeutics, 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/galectin+9+tim3/cell+function+t/pm40999423-484-6-3
Average 86 stars, based on 1 article reviews
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tim3  (Galectin Therapeutics)
86
Galectin Therapeutics tim3
Tim3, supplied by Galectin Therapeutics, 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/galectin+9+tim3/lgals3/bio_rxiv__64898__2026__01__26__701473-32-19-20
Average 86 stars, based on 1 article reviews
tim3 - by Bioz Stars, 2026-09
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immune exhaustion markers  (Galectin Therapeutics)
86
Galectin Therapeutics immune exhaustion markers
Immune Exhaustion Markers, supplied by Galectin Therapeutics, 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/galectin+9+tim3/exhaustion+immune+markers/10__1016_slash_j__jiph__2026__103168-213-27-30
Average 86 stars, based on 1 article reviews
immune exhaustion markers - by Bioz Stars, 2026-09
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t cell costimulatory pathway  (Galectin Therapeutics)
86
Galectin Therapeutics t cell costimulatory pathway
T Cell Costimulatory Pathway, supplied by Galectin Therapeutics, 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/galectin+9+tim3/cell+costimulatory+pathway+t/10__17343_slash_sdutfd__1391007-38-6-0
Average 86 stars, based on 1 article reviews
t cell costimulatory pathway - by Bioz Stars, 2026-09
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dominant driver  (Galectin Therapeutics)
86
Galectin Therapeutics dominant driver
Dominant Driver, supplied by Galectin Therapeutics, 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/galectin+9+tim3/dominant+driver/pmc12960090-169-10-5
Average 86 stars, based on 1 article reviews
dominant driver - by Bioz Stars, 2026-09
86/100 stars
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autocrine loop  (Galectin Therapeutics)
86
Galectin Therapeutics autocrine loop
Autocrine Loop, supplied by Galectin Therapeutics, 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/galectin+9+tim3/autocrine+loop/pm41051510-184-4-1
Average 86 stars, based on 1 article reviews
autocrine loop - by Bioz Stars, 2026-09
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epigenetic memory  (Galectin Therapeutics)
86
Galectin Therapeutics epigenetic memory
Figure 2. Molecular network of chronic inflammation inducing immune cell functional depletion through multidimensional mechanisms. Chronic inflammation activates pro-inflammatory signaling pathways, and the activation of these pathways, IL- 6/JAK/STAT3 and TNF-α/NF-κB, leads to the up-regulation of immune checkpoint molecules, such as PD-1 and TIM-3, which in turn leads to T cell exhaustion. Meanwhile, oxidative stress is exacerbated, and mitochondrial dysfunction occurs in chronic inflammatory environments, and excessive ROS accumulation damages mtDNA, leading to metabolic failure. Not only that <t>epigenetic</t> regulation is also abnormal, for example, DNMT3A deletion results in hypermethylation of the IFN-γ gene and aberrant enrichment of the H3K27me3 modification, which drives T-cell differentiation toward the depleted phenotype. In addition, dynamic interactions between immune cells are involved, with CXCL1 secretion by immunosenescence T cells recruiting MDSCs and differentiation of TAMs to M2 phenotype inhibiting T cell infiltration.
Epigenetic Memory, supplied by Galectin Therapeutics, 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/galectin+9+tim3/epigenetic+memory/10__14336_slash_ad__2025__0471-163-8-5
Average 86 stars, based on 1 article reviews
epigenetic memory - by Bioz Stars, 2026-09
86/100 stars
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anti gal 9  (R&D Systems)
93
R&D Systems anti gal 9
Figure 2. Molecular network of chronic inflammation inducing immune cell functional depletion through multidimensional mechanisms. Chronic inflammation activates pro-inflammatory signaling pathways, and the activation of these pathways, IL- 6/JAK/STAT3 and TNF-α/NF-κB, leads to the up-regulation of immune checkpoint molecules, such as PD-1 and TIM-3, which in turn leads to T cell exhaustion. Meanwhile, oxidative stress is exacerbated, and mitochondrial dysfunction occurs in chronic inflammatory environments, and excessive ROS accumulation damages mtDNA, leading to metabolic failure. Not only that <t>epigenetic</t> regulation is also abnormal, for example, DNMT3A deletion results in hypermethylation of the IFN-γ gene and aberrant enrichment of the H3K27me3 modification, which drives T-cell differentiation toward the depleted phenotype. In addition, dynamic interactions between immune cells are involved, with CXCL1 secretion by immunosenescence T cells recruiting MDSCs and differentiation of TAMs to M2 phenotype inhibiting T cell infiltration.
Anti Gal 9, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/galectin+9+tim3/Human+TIM-3+Antibody/pm28321034-53-35-46
Average 93 stars, based on 1 article reviews
anti gal 9 - by Bioz Stars, 2026-09
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tim 3 fc fusion protein  (R&D Systems)
90
R&D Systems tim 3 fc fusion protein
Figure 2. Molecular network of chronic inflammation inducing immune cell functional depletion through multidimensional mechanisms. Chronic inflammation activates pro-inflammatory signaling pathways, and the activation of these pathways, IL- 6/JAK/STAT3 and TNF-α/NF-κB, leads to the up-regulation of immune checkpoint molecules, such as PD-1 and TIM-3, which in turn leads to T cell exhaustion. Meanwhile, oxidative stress is exacerbated, and mitochondrial dysfunction occurs in chronic inflammatory environments, and excessive ROS accumulation damages mtDNA, leading to metabolic failure. Not only that <t>epigenetic</t> regulation is also abnormal, for example, DNMT3A deletion results in hypermethylation of the IFN-γ gene and aberrant enrichment of the H3K27me3 modification, which drives T-cell differentiation toward the depleted phenotype. In addition, dynamic interactions between immune cells are involved, with CXCL1 secretion by immunosenescence T cells recruiting MDSCs and differentiation of TAMs to M2 phenotype inhibiting T cell infiltration.
Tim 3 Fc Fusion Protein, supplied by R&D Systems, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/galectin+9+tim3/Recombinant+Canine+TIM-3+Fc+Chimera+Protein%2C+CF/pmc06741535-59-5-10
Average 90 stars, based on 1 article reviews
tim 3 fc fusion protein - by Bioz Stars, 2026-09
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interactions promote batf expression  (Galectin Therapeutics)
86
Galectin Therapeutics interactions promote batf expression
Figure 2. Molecular network of chronic inflammation inducing immune cell functional depletion through multidimensional mechanisms. Chronic inflammation activates pro-inflammatory signaling pathways, and the activation of these pathways, IL- 6/JAK/STAT3 and TNF-α/NF-κB, leads to the up-regulation of immune checkpoint molecules, such as PD-1 and TIM-3, which in turn leads to T cell exhaustion. Meanwhile, oxidative stress is exacerbated, and mitochondrial dysfunction occurs in chronic inflammatory environments, and excessive ROS accumulation damages mtDNA, leading to metabolic failure. Not only that <t>epigenetic</t> regulation is also abnormal, for example, DNMT3A deletion results in hypermethylation of the IFN-γ gene and aberrant enrichment of the H3K27me3 modification, which drives T-cell differentiation toward the depleted phenotype. In addition, dynamic interactions between immune cells are involved, with CXCL1 secretion by immunosenescence T cells recruiting MDSCs and differentiation of TAMs to M2 phenotype inhibiting T cell infiltration.
Interactions Promote Batf Expression, supplied by Galectin Therapeutics, 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/galectin+9+tim3/batf+expression+interactions+promote/pmc12436424-32-2-1
Average 86 stars, based on 1 article reviews
interactions promote batf expression - by Bioz Stars, 2026-09
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mbl-cll4  (MBL Life science)
90
MBL Life science mbl-cll4
Figure 2. Molecular network of chronic inflammation inducing immune cell functional depletion through multidimensional mechanisms. Chronic inflammation activates pro-inflammatory signaling pathways, and the activation of these pathways, IL- 6/JAK/STAT3 and TNF-α/NF-κB, leads to the up-regulation of immune checkpoint molecules, such as PD-1 and TIM-3, which in turn leads to T cell exhaustion. Meanwhile, oxidative stress is exacerbated, and mitochondrial dysfunction occurs in chronic inflammatory environments, and excessive ROS accumulation damages mtDNA, leading to metabolic failure. Not only that <t>epigenetic</t> regulation is also abnormal, for example, DNMT3A deletion results in hypermethylation of the IFN-γ gene and aberrant enrichment of the H3K27me3 modification, which drives T-cell differentiation toward the depleted phenotype. In addition, dynamic interactions between immune cells are involved, with CXCL1 secretion by immunosenescence T cells recruiting MDSCs and differentiation of TAMs to M2 phenotype inhibiting T cell infiltration.
Mbl Cll4, supplied by MBL Life science, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/galectin+9+tim3/mbl+cll4/pm35020831-27-189-199
Average 90 stars, based on 1 article reviews
mbl-cll4 - by Bioz Stars, 2026-09
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rkergnostic ma il 10  (Galectin Therapeutics)
86
Galectin Therapeutics rkergnostic ma il 10
Figure 2. Molecular network of chronic inflammation inducing immune cell functional depletion through multidimensional mechanisms. Chronic inflammation activates pro-inflammatory signaling pathways, and the activation of these pathways, IL- 6/JAK/STAT3 and TNF-α/NF-κB, leads to the up-regulation of immune checkpoint molecules, such as PD-1 and TIM-3, which in turn leads to T cell exhaustion. Meanwhile, oxidative stress is exacerbated, and mitochondrial dysfunction occurs in chronic inflammatory environments, and excessive ROS accumulation damages mtDNA, leading to metabolic failure. Not only that <t>epigenetic</t> regulation is also abnormal, for example, DNMT3A deletion results in hypermethylation of the IFN-γ gene and aberrant enrichment of the H3K27me3 modification, which drives T-cell differentiation toward the depleted phenotype. In addition, dynamic interactions between immune cells are involved, with CXCL1 secretion by immunosenescence T cells recruiting MDSCs and differentiation of TAMs to M2 phenotype inhibiting T cell infiltration.
Rkergnostic Ma Il 10, supplied by Galectin Therapeutics, 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/galectin+9+tim3/10+il+ma+rkergnostic/pm41927833-73-53-65
Average 86 stars, based on 1 article reviews
rkergnostic ma il 10 - by Bioz Stars, 2026-09
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Image Search Results


Figure 2. Molecular network of chronic inflammation inducing immune cell functional depletion through multidimensional mechanisms. Chronic inflammation activates pro-inflammatory signaling pathways, and the activation of these pathways, IL- 6/JAK/STAT3 and TNF-α/NF-κB, leads to the up-regulation of immune checkpoint molecules, such as PD-1 and TIM-3, which in turn leads to T cell exhaustion. Meanwhile, oxidative stress is exacerbated, and mitochondrial dysfunction occurs in chronic inflammatory environments, and excessive ROS accumulation damages mtDNA, leading to metabolic failure. Not only that epigenetic regulation is also abnormal, for example, DNMT3A deletion results in hypermethylation of the IFN-γ gene and aberrant enrichment of the H3K27me3 modification, which drives T-cell differentiation toward the depleted phenotype. In addition, dynamic interactions between immune cells are involved, with CXCL1 secretion by immunosenescence T cells recruiting MDSCs and differentiation of TAMs to M2 phenotype inhibiting T cell infiltration.

Journal: Aging and Disease

Article Title: Tumor Immunosenescence Driven by Chronic Inflammation: Mechanisms, Microenvironment Remodeling and Therapeutic Strategies

doi: 10.14336/ad.2025.0471

Figure Lengend Snippet: Figure 2. Molecular network of chronic inflammation inducing immune cell functional depletion through multidimensional mechanisms. Chronic inflammation activates pro-inflammatory signaling pathways, and the activation of these pathways, IL- 6/JAK/STAT3 and TNF-α/NF-κB, leads to the up-regulation of immune checkpoint molecules, such as PD-1 and TIM-3, which in turn leads to T cell exhaustion. Meanwhile, oxidative stress is exacerbated, and mitochondrial dysfunction occurs in chronic inflammatory environments, and excessive ROS accumulation damages mtDNA, leading to metabolic failure. Not only that epigenetic regulation is also abnormal, for example, DNMT3A deletion results in hypermethylation of the IFN-γ gene and aberrant enrichment of the H3K27me3 modification, which drives T-cell differentiation toward the depleted phenotype. In addition, dynamic interactions between immune cells are involved, with CXCL1 secretion by immunosenescence T cells recruiting MDSCs and differentiation of TAMs to M2 phenotype inhibiting T cell infiltration.

Article Snippet: Senescent T cells upregulate the TIM-3/Galectin-9 axis through epigenetic memory, driving YAP nuclear translocation and inducing TOX expression through inhibition of LATS1/2 kinase activity, thereby creating “epigenetic lock-in” of the depletion phenotype [125, 126].

Techniques: Functional Assay, Protein-Protein interactions, Activation Assay, Modification, Cell Differentiation

Figure 3. Multi-level regulatory network of SASP factors and pro-tumorigenic effects. The regulatory network of SASP is complex, on the one hand, the NF-κB and p38 MAPK pathways synergistically regulate the secretion of IL-6, IL-8 and other factors. On the other hand, ATM/ATR, cGAS-STING and NOTCH signaling pathways synergistically enhance the transcription of pro-inflammatory factors. In addition, epigenetic reprogramming is also involved, such as p300-mediated acetylation of H3K27, which amplifies the effects of SASP, which creates a vicious cycle of inflammation-aging-promotion through various mechanisms, such as recruitment of MDSCs, inhibition of dendritic cell antigen presentation, promotion of angiogenesis and metabolic inhibition.

Journal: Aging and Disease

Article Title: Tumor Immunosenescence Driven by Chronic Inflammation: Mechanisms, Microenvironment Remodeling and Therapeutic Strategies

doi: 10.14336/ad.2025.0471

Figure Lengend Snippet: Figure 3. Multi-level regulatory network of SASP factors and pro-tumorigenic effects. The regulatory network of SASP is complex, on the one hand, the NF-κB and p38 MAPK pathways synergistically regulate the secretion of IL-6, IL-8 and other factors. On the other hand, ATM/ATR, cGAS-STING and NOTCH signaling pathways synergistically enhance the transcription of pro-inflammatory factors. In addition, epigenetic reprogramming is also involved, such as p300-mediated acetylation of H3K27, which amplifies the effects of SASP, which creates a vicious cycle of inflammation-aging-promotion through various mechanisms, such as recruitment of MDSCs, inhibition of dendritic cell antigen presentation, promotion of angiogenesis and metabolic inhibition.

Article Snippet: Senescent T cells upregulate the TIM-3/Galectin-9 axis through epigenetic memory, driving YAP nuclear translocation and inducing TOX expression through inhibition of LATS1/2 kinase activity, thereby creating “epigenetic lock-in” of the depletion phenotype [125, 126].

Techniques: Protein-Protein interactions, Inhibition, Immunopeptidomics

Figure 7. Multidimensional intervention strategies for chronic inflammation-driven immunosenescence. For source-targeted intervention, there are anti-IL-6 antibodies, ROS scavengers, and colony transplantation. For SASP network blockade, Senolytics drugs, JAK/STAT inhibitors are available. In terms of combination therapy optimization, combination of epigenetic drugs and immune checkpoint inhibitors and radiotherapy with SASP modulation are common approaches. In addition, there are technological innovations such as CRISPR-edited CAR-T and nano-delivery systems.

Journal: Aging and Disease

Article Title: Tumor Immunosenescence Driven by Chronic Inflammation: Mechanisms, Microenvironment Remodeling and Therapeutic Strategies

doi: 10.14336/ad.2025.0471

Figure Lengend Snippet: Figure 7. Multidimensional intervention strategies for chronic inflammation-driven immunosenescence. For source-targeted intervention, there are anti-IL-6 antibodies, ROS scavengers, and colony transplantation. For SASP network blockade, Senolytics drugs, JAK/STAT inhibitors are available. In terms of combination therapy optimization, combination of epigenetic drugs and immune checkpoint inhibitors and radiotherapy with SASP modulation are common approaches. In addition, there are technological innovations such as CRISPR-edited CAR-T and nano-delivery systems.

Article Snippet: Senescent T cells upregulate the TIM-3/Galectin-9 axis through epigenetic memory, driving YAP nuclear translocation and inducing TOX expression through inhibition of LATS1/2 kinase activity, thereby creating “epigenetic lock-in” of the depletion phenotype [125, 126].

Techniques: Transplantation Assay, CRISPR