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, pr...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.展开更多
基金National Institutes of Health (CCSG CA16672)Cancer Prevention & Research Institutes of Texas (DP150052 and RP160710)+7 种基金National Breast Cancer Foundation, Inc.Breast Cancer Research Foundation (BCRF-17-069)Patel Memorial Breast Cancer Endowment FundThe University of Texas MD Anderson-China Medical University and Hospital Sister Institution FundMinistry of Science and Technology, International Research-intensive Centers of Excellence in Taiwan (I-RiCE MOST 105-2911-I-002-302)Ministry of Health and Welfare, China Medical University Hospital Cancer Research Center of Excellence (MOHW106-TDU-B-212-144003)Center for Biological Pathways
文摘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.
