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Title:
The role of T-cell immunoglobulin mucin-3 and its ligand galectin-9 in antitumor immunity and cancer immunotherapy | Science China Life Sciences
Description:
Cancer treatment in the past few years has been transformed by a new kind of therapy that targets the immune system instead of the cancer itself to reinvigorate antitumor immunity with astonishing results. However, primary and acquired resistance to this type of treatment, namely immune checkpoint blockade (ICB), continue to counter treatment efficacy. In many cases, resistance has been attributed to defective or chronically enhanced interferon signaling and/or upregulation of alternative immune checkpoints, including T-cell immunoglobulin mucin-3 (Tim-3) and its ligand galactin-9 (Gal-9). In this article, we briefly describe the current knowledge of common checkpoint resistance mechanisms, focusing on the Tim-3/Gal-9 pathway as an alternative checkpoint that holds great promise as another target for ICB.
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pubmed, article, google, scholar, cas, cancer, central, cell, immunol, tim, galectin, immune, cells, nat, immunity, immunotherapy, kuchroo, tcell, resistance, rev, lee, hirashima, tumor, type, blockade, regulates, mucin, yang, hung, checkpoint, interferon, signaling, china, access, freeman, sci, anderson, research, ligand, protein, human, usa, wang, med, zhu, schreiber, chen, university, privacy, cookies,
Topics {βοΈ}
ifnΞ³-dependent tissue-immune homeostasis mrl/lpr lupus-prone mice galectin-9-independent ligand-binding surface month download article/chapter suppress t-cell proliferation international research-intensive centers nuclear factor-kappab activation t-cell immunoglobulin mucin-3 mesenchymal stem/stromal cells mien-chie hung cd8 t-cell responses innate immune sensing calcium-calpain-caspase-1 pathway beta-galactoside binding lectin cd8 t-cell exhaustion china life sci regulating anti-tumor immunity china medical university tumor-infiltrating tim-3 virus-specific humoral ifn-Ξ³ pathway genes peritumoral immune tolerance full article pdf cd44 reciprocally regulates growing tumors induce t-cell exhaustion tim-3 mediates phagocytosis tim-3 ligand regulates privacy choices/manage cookies therapeutic pd-1 blockade alternative immune checkpoints article yang immune checkpoint blockade immune-checkpoint blockade related subjects chronic viral infection shape tumour immunogenicity encephalitogenic th1/th17 th1-suppressive effects phosphoinositide 3-kinase pathway experimental autoimmune encephalomyelitis interferon receptor promotes galectin-9 induces apoptosis emerging therapeutic targets phosphotyrosine-dependent coupling immune checkpoint target tim-3/gal-9 pathway impaired interferon signaling common immune defect tumor-intrinsic
Questions {β}
- Antigen-independent induction of Tim-3 expression on human T cells by the common?
- Galectins and immune responses-just how do they do those things they do?
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headline:The role of T-cell immunoglobulin mucin-3 and its ligand galectin-9 in antitumor immunity and cancer immunotherapy
description:Cancer treatment in the past few years has been transformed by a new kind of therapy that targets the immune system instead of the cancer itself to reinvigorate antitumor immunity with astonishing results. However, primary and acquired resistance to this type of treatment, namely immune checkpoint blockade (ICB), continue to counter treatment efficacy. In many cases, resistance has been attributed to defective or chronically enhanced interferon signaling and/or upregulation of alternative immune checkpoints, including T-cell immunoglobulin mucin-3 (Tim-3) and its ligand galactin-9 (Gal-9). In this article, we briefly describe the current knowledge of common checkpoint resistance mechanisms, focusing on the Tim-3/Gal-9 pathway as an alternative checkpoint that holds great promise as another target for ICB.
datePublished:2017-10-11T00:00:00Z
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immune checkpoints
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headline:The role of T-cell immunoglobulin mucin-3 and its ligand galectin-9 in antitumor immunity and cancer immunotherapy
description:Cancer treatment in the past few years has been transformed by a new kind of therapy that targets the immune system instead of the cancer itself to reinvigorate antitumor immunity with astonishing results. However, primary and acquired resistance to this type of treatment, namely immune checkpoint blockade (ICB), continue to counter treatment efficacy. In many cases, resistance has been attributed to defective or chronically enhanced interferon signaling and/or upregulation of alternative immune checkpoints, including T-cell immunoglobulin mucin-3 (Tim-3) and its ligand galactin-9 (Gal-9). In this article, we briefly describe the current knowledge of common checkpoint resistance mechanisms, focusing on the Tim-3/Gal-9 pathway as an alternative checkpoint that holds great promise as another target for ICB.
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