Cellular and molecular mechanisms in cancer immune escape: a comprehensive review

被引:119
作者
Bhatia, Alka [1 ]
Kumar, Yashwant [2 ]
机构
[1] PGIMER, Dept Expt Med & Biotechnol, Chandigarh 160012, India
[2] PGIMER, Dept Immunopathol, Chandigarh 160012, India
关键词
cancer; immune escape; myeloid-derived suppressor cells; protumor; T regulatory cells; REGULATORY T-CELLS; CLASS-I EXPRESSION; TUMOR-INFILTRATING LYMPHOCYTES; FAS-MEDIATED APOPTOSIS; HEAT-SHOCK PROTEINS; GROWTH-FACTOR-BETA; B7; FAMILY-MEMBER; SUPPRESSOR-CELLS; DENDRITIC CELLS; NK CELLS;
D O I
10.1586/1744666X.2014.865519
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Immune escape is the final phase of cancer immunoediting process wherein cancer modulates our immune system to escape from being destroyed by it. Many cellular and molecular events govern the cancer's evasion of host immune response. The tumor undergoes continuous remodeling at the genetic, epigenetic and metabolic level to acquire resistance to apoptosis. At the same time, it effectively modifies all the components of the host's immunome so as to escape from its antitumor effects. Moreover, it induces accumulation of suppressive cells like Treg and myeloid derived suppressor cells and factors which also enable it to elude the immune system. Recent research in this area helps in defining the role of newer players like miRNAs and exosomes in immune escape. The immunotherapeutic approaches developed to target the escape phase appear quite promising; however, the quest for a perfect therapeutic agent that can achieve maximum cure with minimal toxicity continues.
引用
收藏
页码:41 / 62
页数:22
相关论文
共 226 条
[141]   Towards a Genetic Definition of Cancer-Associated Inflammation Role of the IDO Pathway [J].
Prendergast, George C. ;
Metz, Richard ;
Muller, Alexander J. .
AMERICAN JOURNAL OF PATHOLOGY, 2010, 176 (05) :2082-2087
[142]  
Quatromoni JG, 2012, AM J TRANSL RES, V4, P376
[143]   Multiple inhibitory ligands induce impaired T-cell immunologic synapse function in chronic lymphocytic leukemia that can be blocked with lenalidomide: establishing a reversible immune evasion mechanism in human cancer [J].
Ramsay, Alan G. ;
Clear, Andrew J. ;
Fatah, Rewas ;
Gribben, John G. .
BLOOD, 2012, 120 (07) :1412-1421
[144]   Evidence that cervical cancer cells secrete IL-2, which becomes an autocrine growth factor [J].
Rangel-Corona, R. ;
Corona-Ortega, T. ;
Soto-Cruz, I. ;
Lopez-Labra, A. ;
Pablo-Arcos, T. ;
Torres-Guarneros, C. F. ;
Weiss-Steider, B. .
CYTOKINE, 2010, 50 (03) :273-277
[145]  
Rao A, 2010, J IMMUNOL, V184
[146]  
Reichert TE, 2002, CLIN CANCER RES, V8, P3137
[147]   Involvement of cellular death in TRAIL/DR5-dependent suppression induced by CD4+CD25+ regulatory T cells [J].
Ren, X. ;
Ye, F. ;
Jiang, Z. ;
Chu, Y. ;
Xiong, S. ;
Wang, Y. .
CELL DEATH AND DIFFERENTIATION, 2007, 14 (12) :2076-2084
[148]   Immunity to cancer: attack and escape in T lymphocyte-tumor cell interaction [J].
Rivoltini, L ;
Carrabba, M ;
Huber, V ;
Castelli, C ;
Novellino, L ;
Dalerba, P ;
Mortarini, R ;
Arancia, G ;
Anichini, A ;
Fais, S ;
Parmiani, G .
IMMUNOLOGICAL REVIEWS, 2002, 188 :97-113
[149]   Arginine regulation by myeloid derived suppressor cells and tolerance in cancer:: mechanisms and therapeutic perspectives [J].
Rodriguez, Paulo C. ;
Ochoa, Augusto C. .
IMMUNOLOGICAL REVIEWS, 2008, 222 :180-191
[150]   L-arginine availability regulates T-lymphocyte cell-cycle progression [J].
Rodriguez, Paulo C. ;
Quiceno, David G. ;
Ochoa, Augusto C. .
BLOOD, 2007, 109 (04) :1568-1573