Cdk5 disruption attenuates tumor PD-L1 expression and promotes antitumor immunity
| Autor: | Jay Myers, John J. Letterio, Alex Yee-Chen Huang, Steven M. Chirieleison, Deborah S. Barkauskas, Agne Petrosiute, Duncan Stearns, Derek W. Abbott, Joseph Nthale, Stephanie Avril, R. Dixon Dorand, Tej K. Pareek |
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| Rok vydání: | 2016 |
| Předmět: |
CD4-Positive T-Lymphocytes
Male 0301 basic medicine Interferon Regulatory Factor 2 Mice Nude Biology B7-H1 Antigen Article Mice 03 medical and health sciences Cell Line Tumor Animals Humans Cerebellar Neoplasms Immunologic Surveillance Regulation of gene expression Multidisciplinary Kinase Cyclin-dependent kinase 5 Cyclin-Dependent Kinase 5 Neoplasms Experimental Immune checkpoint Gene Expression Regulation Neoplastic Mice Inbred C57BL 030104 developmental biology nervous system Tumor Escape Immunology Cancer research IRF2 Interferon Regulatory Factor-2 Medulloblastoma Transcription Factors Interferon regulatory factors |
| Zdroj: | Science. 353:399-403 |
| ISSN: | 1095-9203 0036-8075 |
| DOI: | 10.1126/science.aae0477 |
| Popis: | Cyclin suppresses antitumor immunity Despite the dramatic success of cancer immunotherapy, many types of cancer do not respond. Understanding why could help us to find ways to enhance the overall responsiveness of tumors to immunotherapies. Dorand et al. report that cyclin-dependent kinase 5 (Cdk5), an enzyme that is highly expressed by neurons in many brain cancers, may dampen the ability of T cells to reject tumors. In a mouse model of medulloblastoma, if tumors were Cdk5 deficient, T cells were able to remove them. This heightened antitumor immunity correlated with reduced expression of the inhibitory molecule programmed cell death ligand 1 (PD-L1), a target of current cancer immunotherapies. Science , this issue p. 399 |
| Databáze: | OpenAIRE |
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