Reserch progress of immune checkpoint molecules and glioma

doi:10.3877/cma.j.issn.2095-9141.2016.06.009

Abstract

Abstract:

With the development of molecular biology and tumor immunology, immunotherapy has gradually developed into an important strategy for cancer treatment in recent years, following surgery, radiotherapy, chemotherapy and targeted therapy. By blocking the immune checkpoint molecules to block certain inhibitory signals pathway, it can activate the immune system, enhance T cell activity, inhibit the immune escape of tumor cells, ultimately inhibit tumor growth and improve patient prognosis. In this paper, we would illustrate the reserch progress of immune checkpoint molecules in glioma.

Key words: Glioma, Immune checkpoint, Immune therapy

Jing Fang, Jinhu Li, Yimin Fan. Reserch progress of immune checkpoint molecules and glioma[J]. Chinese Journal of Neurotraumatic Surgery(Electronic Edition), 2016, 02(06): 361-364.

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https://zhsjcswkdzzz.cma-cmc.com.cn/EN/Y2016/V02/I06/361

References 39

[1]	Saunders NR, Dreifuss JJ, Dziegielewska KM, et al. The rights and wrongs of blood-brain barrier permeability studies: a walk through 100 years of history[J]. Front Neurosci, 2014, 8: 404.
[2]	Davies DC. Blood-brain barrier breakdown in septic encephalopathy and brain tumours[J]. J Anat, 2002, 200(6): 639-646.
[3]	Rascher G, Fischmann A, Kröger S, et al. Extracellular matrix and the blood-brain barrier in glioblastoma multiforme: spatial segregation of tenascin and agrin[J]. Acta Neuropathol, 2002, 104(1): 85-91.
[4]	Reardon DA, Freeman G, Wu C, et al. Immunotherapy advances for glioblastoma[J]. Neuro Oncol, 2014, 16(11): 1441-1458.
[5]	Louveau A, Smirnov I, Keyes TJ, et al. Structural and functional features of central nervous system lymphatic vessels[J]. Nature, 2015, 523(7560): 337-341.
[6]	Dunn GP, Dunn IF, Curry WT. Focus on TILs: Prognostic significance of tumor infiltrating lymphocytes in human glioma[J]. Cancer Immune, 2007, 7: 12.
[7]	Ransohoff RM, Engelhardt B. The anatomical and cellular basis of immune surveillance in the central nervous system[J]. Nat Rev Immunol, 2012, 12(9): 623-635.
[8]	Townsend SE, Allison JP. Tumor rejection after direct costimulation of CD8+ T cells by B7-transfected melanoma cells[J]. Science, 1993, 259(5093): 368-370.
[9]	Driessens G, Kline J, Gajewski TF. Costimulatory and coinhibitory receptors in anti-tumor immunity[J]. Immunol Rev, 2009, 229(1): 126-144.
[10]	See AP, Han JE, Phallen J, et al. The role of STAT3 activation in modulating the immune microenvironment of GBM[J]. J Neurooncol, 2012, 110(3): 359-368.
[11]	Waterhouse P, Penninger JM, Timms E, et al. Lymphoproliferative disorders with early lethality in mice deficient in Ctla-4[J]. Science, 1995, 270(5238): 985-988.
[12]	Quezada SA, Peggs KS, Curran MA, et al. CTLA4 blockade and GM-CSF combination immunotherapy alters the intratumor balance of effector and regulatory T cells[J]. J Clin Invest, 2006. 116(7): 1935-1945.
[13]	Hurwitz AA, Yu TF, Leach DR, et al. CTLA-4 blockade synergizes with tumor-derived granulocyte-macrophage colony-stimulating factor for treatment of an experimental mammary carcinoma[J]. Proc Natl Acad Sci USA, 1998, 95(17): 10067-10071.
[14]	Fecci PE, Ochiai H, Mitchell DA, et al. Systemic CTLA-4 blockade ameliorates glioma-induced changes to the CD4⁺ T cell compartment without affecting regulatory T-cell function[J]. Clin Cancer Res, 2007, 13(7): 2158-2167.
[15]	Wainwright DA, Chang AL, Dey M, et al. Durable therapeutic efficacy utilizing combinatorial blockade against IDO, CTLA-4, and PD-L1 in mice with brain tumors[J]. Clin Cancer Res, 2014, 20(20): 5290-5301.
[16]	Agarwalla P, Barnard Z, Fecci P, et al. Sequential immunotherapy by vaccination with GM-CSF-expressing glioma cells and CTLA-4 blockade effectively treats established murine intracranial tumors[J]. J Immunother, 2012, 35(5): 385-389.
[17]	Carter T, Shaw H, Cohn-Brown D, et al. Ipilimumab and bevacizumab in glioblastoma[J]. Clin Oncol (R Coll Radiol), 2016, pill: S0936-6555(16)30076-0
[18]	Dong H, Strome SE, Salomao DR, et al. Tumor-associated B7-H1 promotes T-cell apoptosis: a potential mechanism of immune evasion[J]. Nat Med, 2002, 8(8): 793-800.
[19]	Keir ME, Butte MJ, Freeman GJ, et al. PD-1 and its ligands in tolerance and immunity[J]. Annu Rev Immunol, 2008, 26: 677-704.
[20]	Topalian SL, Hodi FS, Brahmer JR, et al. Safety, activity, and immune correlates of anti-PD-1 antibody in cancer[J]. N Engl J Med, 2012, 366(26): 2443-2454.
[21]	Jure-Kunkel M, Selby M, Lewis K, et al. Nonclinical evaluation of the combination of mouse IL-21 and anti-mouse CTLA-4 or PD-1 blocking antibodies in mouse tumor models[J]. J Clin Oncol, 2013, 31(15).
[22]	Robert C, Long GV, Brady B, et al. Nivolumab in previously untreated melanoma without BRAF mutation[J]. N Engl J Med, 2015, 372(4): 320-330.
[23]	Berghoff AS, Kiesel B, Widhalm G, et al. Programmed death ligand 1 expression and tumor-infiltrating lymphocytes in glioblastoma[J]. Neuro Oncol, 2015, 17(8): 1064-1075.
[24]	Garber ST, Hashimoto Y, Weathers SP, et al. Immune checkpoint blockade as a potential therapeutic target: surveying CNS malignancies[J]. Neuro Oncol, 2016, pill:now132.
[25]	Huang BY, Zhan YP, Zong WJ, et al. The PD-1/B7-H1 pathway modulates the natural killer cells versus mouse glioma stem cells[J]. PLoS One, 2015, 10(8): e0134715.
[26]	Chen D, Iijima H, Nagaishi T, et al. Carcinoembryonic antigen-related cellular adhesion molecule 1 isoforms alternatively inhibit and costimulate human T cell function[J]. J Immunol, 2004, 172(6): 3535-3543.
[27]	Huang YH, Zhu C, Kondo Y, et al. CEACAM1 regulates TIM-3-mediated tolerance and exhaustion[J]. Nature, 2015, 517(7534): 386-390.
[28]	Ashkenazi S, Ortenberg R, Besser M, et al. SOX9 indirectly regulates CEACAM1 expression and immune resistance in melanoma cells[J]. Oncotarget. 2016.
[29]	Sapoznik S, Hammer O, Ortenberg R, et al. Novel anti-melanoma immunotherapies: disarming tumor escape mechanisms[J]. Clin Dev Immunol, 2012, 2012: 818214.
[30]	Zhang L, Wang J, Wei F, et al. Profiling the dynamic expression of checkpoint molecules on cytokine-induced killer cells from non-small-cell lung cancer patients[J]. Oncotarget, 2016.
[31]	Grosso JF, Kelleher CC, Harris TJ, et al. LAG-3 regulates CD8⁺ T cell accumulation and effector function in murine self-and tumor-tolerance systems. J Clin Invest[J]. 2007. 117(11): 3383-3392.
[32]	Ngiow SF, von SB, Akiba H, et al. Anti-TIM3 antibody promotes T cell IFN-γ-mediated antitumor immunity and suppresses established tumors[J]. Cancer Res, 2011, 71(10): 3540-3551.
[33]	Wainwright DA, Balyasnikova IV, Chang AL, et al. IDO expression in brain tumors increases the recruitment of regulatory T cells and negatively impacts survival[J]. Clin Cancer Res, 2012, 18(22): 6110-6121.
[34]	Moertel CL, Xia J, LaRue R, et al. CD200 in CNS tumor-induced immunosuppression: the role for CD200 pathway blockade in targeted immunotherapy[J]. J Immunother Cancer, 2014. 2(1): 46.
[35]	Sharma P, Allison JP. The future of immune checkpoint therapy[J]. Science, 2015, 348(6230): 56-61.
[36]	Wolchok JD, Kluger H, Callahan MK, et al. Nivolumab plus ipilimumab in advanced melanoma[J]. N Engl J Med, 2013, 369(2): 122-133.
[37]	Curran MA, Montalvo W, Yagita H, et al. PD-1 and CTLA-4 combination blockade expands infiltrating T cells and reduces regulatory T and myeloid cells within B16 melanoma tumors[J]. Proc Natl Acad Sci U S A, 2010, 107(9): 4275-4280.
[38]	Woo SR, Turnis ME, Goldberg MV, et al. Immune inhibitory molecules LAG-3 and PD-1 synergistically regulate T-cell function to promote tumoral immune escape[J]. Cancer Res, 2012, 72(4): 917-927.
[39]	Sakuishi K, Apetoh L, Sullivan JM, et al. Targeting Tim-3 and PD-1 pathways to reverse T cell exhaustion and restore anti-tumor immunity[J]. J Exp Med, 2010, 207(10): 2187-2194.

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