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10.1038/nrc3239

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suck abstract from ncbi


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pmid22437870
      Nat+Rev+Cancer 2012 ; 12 (4 ): 252-64
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  • The blockade of immune checkpoints in cancer immunotherapy #MMPMID22437870
  • Pardoll DM
  • Nat Rev Cancer 2012[Mar]; 12 (4 ): 252-64 PMID22437870 show ga
  • Among the most promising approaches to activating therapeutic antitumour immunity is the blockade of immune checkpoints. Immune checkpoints refer to a plethora of inhibitory pathways hardwired into the immune system that are crucial for maintaining self-tolerance and modulating the duration and amplitude of physiological immune responses in peripheral tissues in order to minimize collateral tissue damage. It is now clear that tumours co-opt certain immune-checkpoint pathways as a major mechanism of immune resistance, particularly against T cells that are specific for tumour antigens. Because many of the immune checkpoints are initiated by ligand-receptor interactions, they can be readily blocked by antibodies or modulated by recombinant forms of ligands or receptors. Cytotoxic T-lymphocyte-associated antigen 4 (CTLA4) antibodies were the first of this class of immunotherapeutics to achieve US Food and Drug Administration (FDA) approval. Preliminary clinical findings with blockers of additional immune-checkpoint proteins, such as programmed cell death protein 1 (PD1), indicate broad and diverse opportunities to enhance antitumour immunity with the potential to produce durable clinical responses.
  • |Animals [MESH]
  • |Antigens, Neoplasm/immunology/metabolism [MESH]
  • |CTLA-4 Antigen/physiology [MESH]
  • |Cancer Vaccines/therapeutic use [MESH]
  • |Clinical Trials as Topic [MESH]
  • |Humans [MESH]
  • |Immunotherapy [MESH]
  • |Molecular Targeted Therapy [MESH]
  • |Neoplasms/immunology/metabolism/*therapy [MESH]
  • |Programmed Cell Death 1 Receptor/physiology [MESH]


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