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<t>ILT4</t> promotes tumour progression directly by inducing malignant behaviors of tumour cells or indirectly by creating immunosuppressive TME. (Left) Tumour-derived ILT4 enhances the proliferation, invasion, migration, and pro-angiogenic ability of tumour cells, meanwhile inhibits their apoptosis via interaction with its ligands HLA-G or ANGPTL2. These abilities of ILT4 directly promote tumour progression. (Right) ILT4 can mediate tumour progression indirectly via creating immunosuppressive TME. ILT4 expression in tumour cells, MDSCs and TAMs induce the recruitment and M2-like polarization of TAMs, which subsequently leads to effector T-cell anergy and Treg proliferation. In addition, ILT4 expression in tumour cells and DCs prevents CD8 + T cell infiltration, induces Treg accumulation, promotes T cell anergy and senescence, and finally impairs the tumoricidal ability of T cells.
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<t>ILT4</t> promotes tumour progression directly by inducing malignant behaviors of tumour cells or indirectly by creating immunosuppressive TME. (Left) Tumour-derived ILT4 enhances the proliferation, invasion, migration, and pro-angiogenic ability of tumour cells, meanwhile inhibits their apoptosis via interaction with its ligands HLA-G or ANGPTL2. These abilities of ILT4 directly promote tumour progression. (Right) ILT4 can mediate tumour progression indirectly via creating immunosuppressive TME. ILT4 expression in tumour cells, MDSCs and TAMs induce the recruitment and M2-like polarization of TAMs, which subsequently leads to effector T-cell anergy and Treg proliferation. In addition, ILT4 expression in tumour cells and DCs prevents CD8 + T cell infiltration, induces Treg accumulation, promotes T cell anergy and senescence, and finally impairs the tumoricidal ability of T cells.
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ILT4 promotes tumour progression directly by inducing malignant behaviors of tumour cells or indirectly by creating immunosuppressive TME. (Left) Tumour-derived ILT4 enhances the proliferation, invasion, migration, and pro-angiogenic ability of tumour cells, meanwhile inhibits their apoptosis via interaction with its ligands HLA-G or ANGPTL2. These abilities of ILT4 directly promote tumour progression. (Right) ILT4 can mediate tumour progression indirectly via creating immunosuppressive TME. ILT4 expression in tumour cells, MDSCs and TAMs induce the recruitment and M2-like polarization of TAMs, which subsequently leads to effector T-cell anergy and Treg proliferation. In addition, ILT4 expression in tumour cells and DCs prevents CD8 + T cell infiltration, induces Treg accumulation, promotes T cell anergy and senescence, and finally impairs the tumoricidal ability of T cells.

Journal: ImmunoTargets and Therapy

Article Title: Targeting ILT4 to Improve Immunotherapy Efficacy in Solid Tumour: From Bench to Bedside

doi: 10.2147/ITT.S548082

Figure Lengend Snippet: ILT4 promotes tumour progression directly by inducing malignant behaviors of tumour cells or indirectly by creating immunosuppressive TME. (Left) Tumour-derived ILT4 enhances the proliferation, invasion, migration, and pro-angiogenic ability of tumour cells, meanwhile inhibits their apoptosis via interaction with its ligands HLA-G or ANGPTL2. These abilities of ILT4 directly promote tumour progression. (Right) ILT4 can mediate tumour progression indirectly via creating immunosuppressive TME. ILT4 expression in tumour cells, MDSCs and TAMs induce the recruitment and M2-like polarization of TAMs, which subsequently leads to effector T-cell anergy and Treg proliferation. In addition, ILT4 expression in tumour cells and DCs prevents CD8 + T cell infiltration, induces Treg accumulation, promotes T cell anergy and senescence, and finally impairs the tumoricidal ability of T cells.

Article Snippet: Based on the synergistic tumoricidal effect of ILT4 and PD-1/PD-L1 blockade, Celldex Therapeutics Company and Biosion jointly developed a bispecific antibody against both ILT4 and PD-1, CDX-585.

Techniques: Derivative Assay, Migration, Expressing

ILT4 blockage improved immunotherapy efficacy. Immunotherapy including anti-PD(L)1 therapy and ACT suppresses tumour progression by reactivating effector or engineered T cells in the TME. However, enriched ILT4 in the tumour cells and TAMs induces the dysfunction or senescence of these T cells, resulting in immunotherapy resistance. While blockade of ILT4 prevents tumour-induced effector and engineered T cells dysfunction, and increases the efficacy of PD(L)1 inhibitors and ACT.

Journal: ImmunoTargets and Therapy

Article Title: Targeting ILT4 to Improve Immunotherapy Efficacy in Solid Tumour: From Bench to Bedside

doi: 10.2147/ITT.S548082

Figure Lengend Snippet: ILT4 blockage improved immunotherapy efficacy. Immunotherapy including anti-PD(L)1 therapy and ACT suppresses tumour progression by reactivating effector or engineered T cells in the TME. However, enriched ILT4 in the tumour cells and TAMs induces the dysfunction or senescence of these T cells, resulting in immunotherapy resistance. While blockade of ILT4 prevents tumour-induced effector and engineered T cells dysfunction, and increases the efficacy of PD(L)1 inhibitors and ACT.

Article Snippet: Based on the synergistic tumoricidal effect of ILT4 and PD-1/PD-L1 blockade, Celldex Therapeutics Company and Biosion jointly developed a bispecific antibody against both ILT4 and PD-1, CDX-585.

Techniques:

ILT4 promotes tumour progression directly by inducing malignant behaviors of tumour cells or indirectly by creating immunosuppressive TME. (Left) Tumour-derived ILT4 enhances the proliferation, invasion, migration, and pro-angiogenic ability of tumour cells, meanwhile inhibits their apoptosis via interaction with its ligands HLA-G or ANGPTL2. These abilities of ILT4 directly promote tumour progression. (Right) ILT4 can mediate tumour progression indirectly via creating immunosuppressive TME. ILT4 expression in tumour cells, MDSCs and TAMs induce the recruitment and M2-like polarization of TAMs, which subsequently leads to effector T-cell anergy and Treg proliferation. In addition, ILT4 expression in tumour cells and DCs prevents CD8 + T cell infiltration, induces Treg accumulation, promotes T cell anergy and senescence, and finally impairs the tumoricidal ability of T cells.

Journal: ImmunoTargets and Therapy

Article Title: Targeting ILT4 to Improve Immunotherapy Efficacy in Solid Tumour: From Bench to Bedside

doi: 10.2147/ITT.S548082

Figure Lengend Snippet: ILT4 promotes tumour progression directly by inducing malignant behaviors of tumour cells or indirectly by creating immunosuppressive TME. (Left) Tumour-derived ILT4 enhances the proliferation, invasion, migration, and pro-angiogenic ability of tumour cells, meanwhile inhibits their apoptosis via interaction with its ligands HLA-G or ANGPTL2. These abilities of ILT4 directly promote tumour progression. (Right) ILT4 can mediate tumour progression indirectly via creating immunosuppressive TME. ILT4 expression in tumour cells, MDSCs and TAMs induce the recruitment and M2-like polarization of TAMs, which subsequently leads to effector T-cell anergy and Treg proliferation. In addition, ILT4 expression in tumour cells and DCs prevents CD8 + T cell infiltration, induces Treg accumulation, promotes T cell anergy and senescence, and finally impairs the tumoricidal ability of T cells.

Article Snippet: In 2018, Merck & Co carried out the first clinical trial on the therapeutic ILT4 monoclonal antibody MK-4830 (ClinicalTrials.gov ID: NCT03564691 ).

Techniques: Derivative Assay, Migration, Expressing

ILT4 blockage improved immunotherapy efficacy. Immunotherapy including anti-PD(L)1 therapy and ACT suppresses tumour progression by reactivating effector or engineered T cells in the TME. However, enriched ILT4 in the tumour cells and TAMs induces the dysfunction or senescence of these T cells, resulting in immunotherapy resistance. While blockade of ILT4 prevents tumour-induced effector and engineered T cells dysfunction, and increases the efficacy of PD(L)1 inhibitors and ACT.

Journal: ImmunoTargets and Therapy

Article Title: Targeting ILT4 to Improve Immunotherapy Efficacy in Solid Tumour: From Bench to Bedside

doi: 10.2147/ITT.S548082

Figure Lengend Snippet: ILT4 blockage improved immunotherapy efficacy. Immunotherapy including anti-PD(L)1 therapy and ACT suppresses tumour progression by reactivating effector or engineered T cells in the TME. However, enriched ILT4 in the tumour cells and TAMs induces the dysfunction or senescence of these T cells, resulting in immunotherapy resistance. While blockade of ILT4 prevents tumour-induced effector and engineered T cells dysfunction, and increases the efficacy of PD(L)1 inhibitors and ACT.

Article Snippet: In 2018, Merck & Co carried out the first clinical trial on the therapeutic ILT4 monoclonal antibody MK-4830 (ClinicalTrials.gov ID: NCT03564691 ).

Techniques: