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Structured Review

Galectin Therapeutics tim 3 ligands
Factors influencing the exhausted state of NK cells. The exhaustion of NK cells in the TME is regulated by multiple factors which results in NK cell function impairment due to: the downregulated expression of NK cell-activating receptors (e.g., NKG2D, DNAM-1, NKp30), the reduced secretion of effector cytokines (such as IFN-γ), and the upregulated expression of immunosuppressive molecules (e.g., PD-1, NKG2A, TIGIT, CD96, <t>TIM-3,</t> LAG-3). Additionally, transforming growth factor-β (TGF-β) secreted by tumor cells, cancer-associated fibroblasts (CAFs), and extracellular vesicles (EVs); hypoxic microenvironment; indoleamine 2,3-dioxygenase (IDO); prostaglandin E2 (PGE2); and immunosuppressive cells including macrophages, regulatory T cells (Treg), and myeloid-derived suppressor cells (MDSC) are involved in regulating NK cell exhaustion through multiple pathways.
Tim 3 Ligands, 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/3/pmc12964005-330-0-2
Average 86 stars, based on 1 article reviews
tim 3 ligands - by Bioz Stars, 2026-11
86/100 stars

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1) Product Images from "Mechanisms of tumor cell evasion from NK cell-mediated killing and advances in NK cell-based cancer immunotherapy"

Article Title: Mechanisms of tumor cell evasion from NK cell-mediated killing and advances in NK cell-based cancer immunotherapy

Journal: Pharmaceutical Science Advances

doi: 10.1016/j.pscia.2026.100109

Factors influencing the exhausted state of NK cells. The exhaustion of NK cells in the TME is regulated by multiple factors which results in NK cell function impairment due to: the downregulated expression of NK cell-activating receptors (e.g., NKG2D, DNAM-1, NKp30), the reduced secretion of effector cytokines (such as IFN-γ), and the upregulated expression of immunosuppressive molecules (e.g., PD-1, NKG2A, TIGIT, CD96, TIM-3, LAG-3). Additionally, transforming growth factor-β (TGF-β) secreted by tumor cells, cancer-associated fibroblasts (CAFs), and extracellular vesicles (EVs); hypoxic microenvironment; indoleamine 2,3-dioxygenase (IDO); prostaglandin E2 (PGE2); and immunosuppressive cells including macrophages, regulatory T cells (Treg), and myeloid-derived suppressor cells (MDSC) are involved in regulating NK cell exhaustion through multiple pathways.
Figure Legend Snippet: Factors influencing the exhausted state of NK cells. The exhaustion of NK cells in the TME is regulated by multiple factors which results in NK cell function impairment due to: the downregulated expression of NK cell-activating receptors (e.g., NKG2D, DNAM-1, NKp30), the reduced secretion of effector cytokines (such as IFN-γ), and the upregulated expression of immunosuppressive molecules (e.g., PD-1, NKG2A, TIGIT, CD96, TIM-3, LAG-3). Additionally, transforming growth factor-β (TGF-β) secreted by tumor cells, cancer-associated fibroblasts (CAFs), and extracellular vesicles (EVs); hypoxic microenvironment; indoleamine 2,3-dioxygenase (IDO); prostaglandin E2 (PGE2); and immunosuppressive cells including macrophages, regulatory T cells (Treg), and myeloid-derived suppressor cells (MDSC) are involved in regulating NK cell exhaustion through multiple pathways.

Techniques Used: Cell Function Assay, Expressing, Derivative Assay

Strategies for enhancing NK cell anti-tumor activity. The anti-tumor efficacy of NK cells can be improved through multiple approaches: Adoptive NK cell infusions, including autologous NK cells (combined with HAIC), allogeneic NK cells (with high potential), and infusions with or without allogeneic transplantation; NK cell checkpoint inhibitors targeting molecules such as PD-1/PD-L1, KIRs (KIR2DL1/2/3/5), NKG2A/CD94, TIM-3, and LAG-3; Advanced applications of CAR-NK cells, including IL-15-secreting CAR-NK cell therapy targeting mesothelin, TIPE2 gene-knockout CAR-NK therapy, and application of modified CCCR-NK92; Administration of stimulatory cytokines like IL-2, IL-15, IL-18, and IL-21; Bi or trispecific killer engagers, including Bispecific antibody: LB1410 (anti-PD-1/TIM-3) and trispecific nanobody: PDL1/PD-1/NKG2A.
Figure Legend Snippet: Strategies for enhancing NK cell anti-tumor activity. The anti-tumor efficacy of NK cells can be improved through multiple approaches: Adoptive NK cell infusions, including autologous NK cells (combined with HAIC), allogeneic NK cells (with high potential), and infusions with or without allogeneic transplantation; NK cell checkpoint inhibitors targeting molecules such as PD-1/PD-L1, KIRs (KIR2DL1/2/3/5), NKG2A/CD94, TIM-3, and LAG-3; Advanced applications of CAR-NK cells, including IL-15-secreting CAR-NK cell therapy targeting mesothelin, TIPE2 gene-knockout CAR-NK therapy, and application of modified CCCR-NK92; Administration of stimulatory cytokines like IL-2, IL-15, IL-18, and IL-21; Bi or trispecific killer engagers, including Bispecific antibody: LB1410 (anti-PD-1/TIM-3) and trispecific nanobody: PDL1/PD-1/NKG2A.

Techniques Used: Activity Assay, Transplantation Assay, Gene Knockout, Modification

Related Articles

Binding Assay:

Article Title: Mechanisms of tumor cell evasion from NK cell-mediated killing and advances in NK cell-based cancer immunotherapy
Article Snippet: TIM-3 ligands-including Galectin-9, PS, HMGB1, and CEACAM-1-play crucial roles in regulating NK activity. .. In AML, Galectin-9 is markedly overexpressed in tumor cells, and its binding to TIM-3 strongly suppresses NK cell activity and IL-2 secretion [ ]. ..

Article Title: Remodeling memory T cells with chemotherapy and immune checkpoint inhibitors as host pre-conditioning to empower in vivo CAR-T therapy
Article Snippet: .. For example, T cells of patients with B-NHL show upregulated pro-exhaustion genes (e.g., galectin 1 [ LGALS1 ]) and downregulated pro-survival genes (e.g., human immunodeficiency virus type I enhancer binding protein 2 [ HIVEP2 ]) after chemotherapy. ..

Activity Assay:

Article Title: Mechanisms of tumor cell evasion from NK cell-mediated killing and advances in NK cell-based cancer immunotherapy
Article Snippet: TIM-3 ligands-including Galectin-9, PS, HMGB1, and CEACAM-1-play crucial roles in regulating NK activity. .. In AML, Galectin-9 is markedly overexpressed in tumor cells, and its binding to TIM-3 strongly suppresses NK cell activity and IL-2 secretion [ ]. ..

Article Title: Mechanisms of tumor cell evasion from NK cell-mediated killing and advances in NK cell-based cancer immunotherapy
Article Snippet: .. TIM-3 ligands-including Galectin-9, PS, HMGB1, and CEACAM-1-play crucial roles in regulating NK activity. .. In AML, Galectin-9 is markedly overexpressed in tumor cells, and its binding to TIM-3 strongly suppresses NK cell activity and IL-2 secretion [ ].

Gas Chromatography:

Article Title: Gastric cancer-secreted galectin-1 promotes peritoneal mesothelial-mesenchymal transition to prime peritoneal metastasis soil
Article Snippet: .. Galectin-1 in the GC microenvironment reprograms peritoneal mesothelial cells to facilitate PM, with its high expression in GC tissues being a key factor for PM. .. Galectin-1-induced peritoneal MMT through the TGF-β/Smad signaling pathway is an important mechanism for GCPM, offering a potential target for GC treatment.

Expressing:

Article Title: Gastric cancer-secreted galectin-1 promotes peritoneal mesothelial-mesenchymal transition to prime peritoneal metastasis soil
Article Snippet: .. Galectin-1 in the GC microenvironment reprograms peritoneal mesothelial cells to facilitate PM, with its high expression in GC tissues being a key factor for PM. .. Galectin-1-induced peritoneal MMT through the TGF-β/Smad signaling pathway is an important mechanism for GCPM, offering a potential target for GC treatment.

other:

Article Title: Beyond eGFR and Albuminuria: Biological Pathways and Multiomics in Cardiovascular–Kidney–Metabolic Disease
Article Snippet: Galectin-3 , Plasma , ELISA , Prospective cohort , HF, CKD fibrotic endotype.

Virus:

Article Title: Remodeling memory T cells with chemotherapy and immune checkpoint inhibitors as host pre-conditioning to empower in vivo CAR-T therapy
Article Snippet: .. For example, T cells of patients with B-NHL show upregulated pro-exhaustion genes (e.g., galectin 1 [ LGALS1 ]) and downregulated pro-survival genes (e.g., human immunodeficiency virus type I enhancer binding protein 2 [ HIVEP2 ]) after chemotherapy. ..



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Factors influencing the exhausted state of NK cells. The exhaustion of NK cells in the TME is regulated by multiple factors which results in NK cell function impairment due to: the downregulated expression of NK cell-activating receptors (e.g., NKG2D, DNAM-1, NKp30), the reduced secretion of effector cytokines (such as IFN-γ), and the upregulated expression of immunosuppressive molecules (e.g., PD-1, NKG2A, TIGIT, CD96, <t>TIM-3,</t> LAG-3). Additionally, transforming growth factor-β (TGF-β) secreted by tumor cells, cancer-associated fibroblasts (CAFs), and extracellular vesicles (EVs); hypoxic microenvironment; indoleamine 2,3-dioxygenase (IDO); prostaglandin E2 (PGE2); and immunosuppressive cells including macrophages, regulatory T cells (Treg), and myeloid-derived suppressor cells (MDSC) are involved in regulating NK cell exhaustion through multiple pathways.
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Factors influencing the exhausted state of NK cells. The exhaustion of NK cells in the TME is regulated by multiple factors which results in NK cell function impairment due to: the downregulated expression of NK cell-activating receptors (e.g., NKG2D, DNAM-1, NKp30), the reduced secretion of effector cytokines (such as IFN-γ), and the upregulated expression of immunosuppressive molecules (e.g., PD-1, NKG2A, TIGIT, CD96, <t>TIM-3,</t> LAG-3). Additionally, transforming growth factor-β (TGF-β) secreted by tumor cells, cancer-associated fibroblasts (CAFs), and extracellular vesicles (EVs); hypoxic microenvironment; indoleamine 2,3-dioxygenase (IDO); prostaglandin E2 (PGE2); and immunosuppressive cells including macrophages, regulatory T cells (Treg), and myeloid-derived suppressor cells (MDSC) are involved in regulating NK cell exhaustion through multiple pathways.
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Factors influencing the exhausted state of NK cells. The exhaustion of NK cells in the TME is regulated by multiple factors which results in NK cell function impairment due to: the downregulated expression of NK cell-activating receptors (e.g., NKG2D, DNAM-1, NKp30), the reduced secretion of effector cytokines (such as IFN-γ), and the upregulated expression of immunosuppressive molecules (e.g., PD-1, NKG2A, TIGIT, CD96, TIM-3, LAG-3). Additionally, transforming growth factor-β (TGF-β) secreted by tumor cells, cancer-associated fibroblasts (CAFs), and extracellular vesicles (EVs); hypoxic microenvironment; indoleamine 2,3-dioxygenase (IDO); prostaglandin E2 (PGE2); and immunosuppressive cells including macrophages, regulatory T cells (Treg), and myeloid-derived suppressor cells (MDSC) are involved in regulating NK cell exhaustion through multiple pathways.

Journal: Pharmaceutical Science Advances

Article Title: Mechanisms of tumor cell evasion from NK cell-mediated killing and advances in NK cell-based cancer immunotherapy

doi: 10.1016/j.pscia.2026.100109

Figure Lengend Snippet: Factors influencing the exhausted state of NK cells. The exhaustion of NK cells in the TME is regulated by multiple factors which results in NK cell function impairment due to: the downregulated expression of NK cell-activating receptors (e.g., NKG2D, DNAM-1, NKp30), the reduced secretion of effector cytokines (such as IFN-γ), and the upregulated expression of immunosuppressive molecules (e.g., PD-1, NKG2A, TIGIT, CD96, TIM-3, LAG-3). Additionally, transforming growth factor-β (TGF-β) secreted by tumor cells, cancer-associated fibroblasts (CAFs), and extracellular vesicles (EVs); hypoxic microenvironment; indoleamine 2,3-dioxygenase (IDO); prostaglandin E2 (PGE2); and immunosuppressive cells including macrophages, regulatory T cells (Treg), and myeloid-derived suppressor cells (MDSC) are involved in regulating NK cell exhaustion through multiple pathways.

Article Snippet: TIM-3 ligands-including Galectin-9, PS, HMGB1, and CEACAM-1-play crucial roles in regulating NK activity.

Techniques: Cell Function Assay, Expressing, Derivative Assay

Strategies for enhancing NK cell anti-tumor activity. The anti-tumor efficacy of NK cells can be improved through multiple approaches: Adoptive NK cell infusions, including autologous NK cells (combined with HAIC), allogeneic NK cells (with high potential), and infusions with or without allogeneic transplantation; NK cell checkpoint inhibitors targeting molecules such as PD-1/PD-L1, KIRs (KIR2DL1/2/3/5), NKG2A/CD94, TIM-3, and LAG-3; Advanced applications of CAR-NK cells, including IL-15-secreting CAR-NK cell therapy targeting mesothelin, TIPE2 gene-knockout CAR-NK therapy, and application of modified CCCR-NK92; Administration of stimulatory cytokines like IL-2, IL-15, IL-18, and IL-21; Bi or trispecific killer engagers, including Bispecific antibody: LB1410 (anti-PD-1/TIM-3) and trispecific nanobody: PDL1/PD-1/NKG2A.

Journal: Pharmaceutical Science Advances

Article Title: Mechanisms of tumor cell evasion from NK cell-mediated killing and advances in NK cell-based cancer immunotherapy

doi: 10.1016/j.pscia.2026.100109

Figure Lengend Snippet: Strategies for enhancing NK cell anti-tumor activity. The anti-tumor efficacy of NK cells can be improved through multiple approaches: Adoptive NK cell infusions, including autologous NK cells (combined with HAIC), allogeneic NK cells (with high potential), and infusions with or without allogeneic transplantation; NK cell checkpoint inhibitors targeting molecules such as PD-1/PD-L1, KIRs (KIR2DL1/2/3/5), NKG2A/CD94, TIM-3, and LAG-3; Advanced applications of CAR-NK cells, including IL-15-secreting CAR-NK cell therapy targeting mesothelin, TIPE2 gene-knockout CAR-NK therapy, and application of modified CCCR-NK92; Administration of stimulatory cytokines like IL-2, IL-15, IL-18, and IL-21; Bi or trispecific killer engagers, including Bispecific antibody: LB1410 (anti-PD-1/TIM-3) and trispecific nanobody: PDL1/PD-1/NKG2A.

Article Snippet: TIM-3 ligands-including Galectin-9, PS, HMGB1, and CEACAM-1-play crucial roles in regulating NK activity.

Techniques: Activity Assay, Transplantation Assay, Gene Knockout, Modification