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PMID: 26272491 Published · ppublish English Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Review

Adaptive Immune Resistance: How Cancer Protects from Immune Attack.

Cancer discovery ·Vol. 5 ·No. 9 ·2015-09-00 ·Pages 915-9

Ribas A

Abstract

Adaptive immune resistance is a process in which the cancer changes its phenotype in response to a cytotoxic or proinflammatory immune response, thereby evading it. This adaptive process is triggered by the specific recognition of cancer cells by T cells, which leads to the production of immune-activating cytokines. Cancers then hijack mechanisms developed to limit inflammatory and immune responses and protect themselves from the T-cell attack. Inhibiting adaptive immune resistance is the mechanistic basis of responses to PD-1 or PD-L1-blocking antibodies, and may be of relevance for the development of other cancer immunotherapy strategies. Several new immunotherapy strategies to treat cancer are based on inhibiting processes through which cancer adapts and evades from an immune response. Recognizing the specific adaptive resistance mechanisms in each case is likely to allow the personalized development of immunotherapies tailored to block how a particular cancer protects itself from the immune system.

MeSH Terms
Adaptive Immunity Animals Antigens, Neoplasm/immunology,metabolism Clinical Decision-Making Cytokines/metabolism Humans Inflammation Mediators/metabolism Neoplasms/diagnosis,immunology,metabolism,therapy T-Lymphocyte Subsets/immunology,metabolism Tumor Escape/immunology
Chemicals
Antigens, Neoplasm Cytokines Inflammation Mediators
Authors & Affiliations
1 authors, click to expand affiliations / ORCID
Ribas Antoni
Division of Hematology-Oncology, Department of Medicine, Jonsson Comprehensive Cancer Center at the University of California, Los Angeles, Los Angeles, California. aribas@mednet.ucla.edu.
References (46)
46 references, click to expand
  1. Predictive correlates of response to the anti-PD-L1 antibody MPDL3280A in cancer patients.
    Nature. 2014 Nov 27;515(7528):563-7 PMID: 25428504
  2. PD-L1 and PD-L2 are differentially regulated by Th1 and Th2 cells.
    Proc Natl Acad Sci U S A. 2003 Apr 29;100(9):5336-41 PMID: 12697896
  3. Immune cell-poor melanomas benefit from PD-1 blockade after targeted type I IFN activation.
    Cancer Discov. 2014 Jun;4(6):674-87 PMID: 24589924
  4. CEACAM1 regulates TIM-3-mediated tolerance and exhaustion.
    Nature. 2015 Jan 15;517(7534):386-90 PMID: 25363763
  5. Reversal of the TCR stop signal by CTLA-4.
    Science. 2006 Sep 29;313(5795):1972-5 PMID: 16931720
  6. Integrative analysis reveals selective 9p24.1 amplification, increased PD-1 ligand expression, and further induction via JAK2 in nodular sclerosing Hodgkin lymphoma and primary mediastinal large B-cell lymphoma.
    Blood. 2010 Oct 28;116(17):3268-77 PMID: 20628145
  7. CTLA4 blockade induces frequent tumor infiltration by activated lymphocytes regardless of clinical responses in humans.
    Clin Cancer Res. 2011 Jun 15;17(12):4101-9 PMID: 21558401
  8. Immunoediting of cancers may lead to epithelial to mesenchymal transition.
    J Immunol. 2006 Aug 1;177(3):1526-33 PMID: 16849459
  9. Effects of MAPK and PI3K pathways on PD-L1 expression in melanoma.
    Clin Cancer Res. 2014 Jul 1;20(13):3446-57 PMID: 24812408
  10. PD-1 blockade induces responses by inhibiting adaptive immune resistance.
    Nature. 2014 Nov 27;515(7528):568-71 PMID: 25428505
  11. Activation of the PD-1 pathway contributes to immune escape in EGFR-driven lung tumors.
    Cancer Discov. 2013 Dec;3(12):1355-63 PMID: 24078774
  12. The basics of epithelial-mesenchymal transition.
    J Clin Invest. 2009 Jun;119(6):1420-8 PMID: 19487818
  13. The future of cancer therapy: selecting patients likely to respond to PD1/L1 blockade.
    Clin Cancer Res. 2014 Oct 1;20(19):4982-4 PMID: 24970841
  14. Cancer therapy: Tumours switch to resist.
    Nature. 2012 Oct 18;490(7420):347-8 PMID: 23051745
  15. CTLA-4-mediated inhibition in regulation of T cell responses: mechanisms and manipulation in tumor immunotherapy.
    Annu Rev Immunol. 2001;19:565-94 PMID: 11244047
  16. Nivolumab and ipilimumab versus ipilimumab in untreated melanoma.
    N Engl J Med. 2015 May 21;372(21):2006-17 PMID: 25891304
  17. Inflammation and cancer.
    Nature. 2002 Dec 19-26;420(6917):860-7 PMID: 12490959
  18. Cancer immunoediting: integrating immunity's roles in cancer suppression and promotion.
    Science. 2011 Mar 25;331(6024):1565-70 PMID: 21436444
  19. Dynamic expression of protective CEACAM1 on melanoma cells during specific immune attack.
    Immunology. 2009 Feb;126(2):186-200 PMID: 18557789
  20. Interferon regulatory factor-1 is prerequisite to the constitutive expression and IFN-gamma-induced upregulation of B7-H1 (CD274).
    FEBS Lett. 2006 Feb 6;580(3):755-62 PMID: 16413538
  21. PD-1 blockade with nivolumab in relapsed or refractory Hodgkin's lymphoma.
    N Engl J Med. 2015 Jan 22;372(4):311-9 PMID: 25482239
  22. Loss of tumor suppressor PTEN function increases B7-H1 expression and immunoresistance in glioma.
    Nat Med. 2007 Jan;13(1):84-8 PMID: 17159987
  23. Molecular and genetic properties of tumors associated with local immune cytolytic activity.
    Cell. 2015 Jan 15;160(1-2):48-61 PMID: 25594174
  24. Intestinal tumorigenesis initiated by dedifferentiation and acquisition of stem-cell-like properties.
    Cell. 2013 Jan 17;152(1-2):25-38 PMID: 23273993
  25. Regulation of PD-1, PD-L1, and PD-L2 expression during normal and autoimmune responses.
    Eur J Immunol. 2003 Oct;33(10):2706-16 PMID: 14515254
  26. Nivolumab in previously untreated melanoma without BRAF mutation.
    N Engl J Med. 2015 Jan 22;372(4):320-30 PMID: 25399552
  27. The blockade of immune checkpoints in cancer immunotherapy.
    Nat Rev Cancer. 2012 Apr;12(4):252-64 PMID: 22437870
  28. Melanocyte lineage-specific antigen gp100 is recognized by melanoma-derived tumor-infiltrating lymphocytes.
    J Exp Med. 1994 Mar 1;179(3):1005-9 PMID: 8113668
  29. The AP1-dependent secretion of galectin-1 by Reed Sternberg cells fosters immune privilege in classical Hodgkin lymphoma.
    Proc Natl Acad Sci U S A. 2007 Aug 7;104(32):13134-9 PMID: 17670934
  30. PD-L1/B7H-1 inhibits the effector phase of tumor rejection by T cell receptor (TCR) transgenic CD8+ T cells.
    Cancer Res. 2004 Feb 1;64(3):1140-5 PMID: 14871849
  31. Pembrolizumab versus Ipilimumab in Advanced Melanoma.
    N Engl J Med. 2015 Jun 25;372(26):2521-32 PMID: 25891173
  32. Up-regulation of PD-L1, IDO, and T(regs) in the melanoma tumor microenvironment is driven by CD8(+) T cells.
    Sci Transl Med. 2013 Aug 28;5(200):200ra116 PMID: 23986400
  33. Gene signature in melanoma associated with clinical activity: a potential clue to unlock cancer immunotherapy.
    Cancer J. 2010 Jul-Aug;16(4):399-403 PMID: 20693853
  34. Immune-induced epithelial to mesenchymal transition in vivo generates breast cancer stem cells.
    Cancer Res. 2009 Apr 1;69(7):2887-95 PMID: 19276366
  35. Plasticity of tumour and immune cells: a source of heterogeneity and a cause for therapy resistance?
    Nat Rev Cancer. 2013 May;13(5):365-76 PMID: 23535846
  36. Cancer exome analysis reveals a T-cell-dependent mechanism of cancer immunoediting.
    Nature. 2012 Feb 16;482(7385):400-4 PMID: 22318521
  37. The three Es of cancer immunoediting.
    Annu Rev Immunol. 2004;22:329-60 PMID: 15032581
  38. Classifying Cancers Based on T-cell Infiltration and PD-L1.
    Cancer Res. 2015 Jun 1;75(11):2139-45 PMID: 25977340
  39. IFNgamma and lymphocytes prevent primary tumour development and shape tumour immunogenicity.
    Nature. 2001 Apr 26;410(6832):1107-11 PMID: 11323675
  40. Combined Nivolumab and Ipilimumab or Monotherapy in Untreated Melanoma.
    N Engl J Med. 2015 Jul 2;373(1):23-34 PMID: 26027431
  41. Colocalization of inflammatory response with B7-h1 expression in human melanocytic lesions supports an adaptive resistance mechanism of immune escape.
    Sci Transl Med. 2012 Mar 28;4(127):127ra37 PMID: 22461641
  42. Constitutive and inducible expression of b7 family of ligands by human airway epithelial cells.
    Am J Respir Cell Mol Biol. 2005 Sep;33(3):280-9 PMID: 15961727
  43. Phenotype switching in melanoma: implications for progression and therapy.
    Front Oncol. 2015 Feb 13;5:31 PMID: 25763355
  44. Gene therapy with human and mouse T-cell receptors mediates cancer regression and targets normal tissues expressing cognate antigen.
    Blood. 2009 Jul 16;114(3):535-46 PMID: 19451549
  45. In vivo switching of human melanoma cells between proliferative and invasive states.
    Cancer Res. 2008 Feb 1;68(3):650-6 PMID: 18245463
  46. Melanomas resist T-cell therapy through inflammation-induced reversible dedifferentiation.
    Nature. 2012 Oct 18;490(7420):412-6 PMID: 23051752
Article Info
Journal
Cancer discovery
Abbr.
Cancer Discov
ISSN
2159-8290
Published
2015-09-00
Epub
2015-00-13
Pages
915-9
Language
English
Region
United States
NLM ID
101561693
PMCID
PMC4560619
Subset
IM
Grants
NCI NIH HHS · R01 CA199205 · United States
NCI NIH HHS · U54 CA119347 · United States
NCI NIH HHS · R35CA197633 · United States
NCI NIH HHS · R01 CA170689 · United States
NCI NIH HHS · P01 CA168585 · United States
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