PMID- 27659281
OWN - NLM
STAT- MEDLINE
DCOM- 20180117
LR  - 20180127
IS  - 2059-2310 (Electronic)
IS  - 2059-2302 (Linking)
VI  - 88
IP  - 5
DP  - 2016 Nov
TI  - Molecular mechanisms of HLA class I-mediated immune evasion of human tumors and 
      their role in resistance to immunotherapies.
PG  - 213-220
LID - 10.1111/tan.12898 [doi]
AB  - Although the human immune system can recognize and eradicate tumor cells, tumors 
      have also been shown to develop different strategies to escape immune 
      surveillance, which has been described for the first time in different mouse 
      models. The evasion of immune recognition was often associated with a poor 
      prognosis and reduced survival of patients. During the last years the molecular 
      mechanisms, which protect tumor cells from this immune attack, have been 
      identified and appear to be more complex than initially expected. However, next 
      to the composition of cellular, soluble and physical components of the tumor 
      microenvironment, the tumor cells changes to limit immune responses. Of 
      particular importance are classical and non-classical human leukocyte antigen 
      (HLA) class I antigens, which often showed a deregulated expression in cancers of 
      distinct origin. Furthermore, HLA class I abnormalities were linked to defects in 
      the interferon signaling, which have both been shown to be essential for mounting 
      immune responses and are involved in resistances to T cell-based immunotherapies. 
      Therefore this review summarizes the expression, regulation, function and 
      clinical relevance of HLA class I antigens in association with the interferon 
      signal transduction pathway and its role in adaptive resistances to 
      immunotherapies.
CI  - (c) 2016 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.
FAU - Seliger, B
AU  - Seliger B
AD  - Institute of Medical Immunology, Martin-Luther-University Halle-Wittenberg, 
      Halle, Germany. Barbara.Seliger@uk-halle.de.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20160922
PL  - England
TA  - HLA
JT  - HLA
JID - 101675570
RN  - 0 (B7-H1 Antigen)
RN  - 0 (CD274 protein, human)
RN  - 0 (Histocompatibility Antigens Class I)
RN  - 0 (PDCD1 protein, human)
RN  - 0 (Programmed Cell Death 1 Receptor)
RN  - 9008-11-1 (Interferons)
SB  - IM
MH  - Animals
MH  - B7-H1 Antigen/genetics/immunology
MH  - Gene Expression Regulation
MH  - Histocompatibility Antigens Class I/genetics/*immunology
MH  - Humans
MH  - *Immune Evasion
MH  - Immunologic Surveillance
MH  - Immunotherapy/*methods
MH  - Interferons/genetics/*immunology
MH  - Mice
MH  - Neoplasms/genetics/*immunology/pathology/therapy
MH  - Programmed Cell Death 1 Receptor/genetics/immunology
MH  - Signal Transduction
MH  - T-Lymphocytes/immunology/pathology
MH  - Tumor Microenvironment/*immunology
OTO - NOTNLM
OT  - T cells
OT  - human leukocyte antigen
OT  - immune suppression
OT  - immune surveillance
OT  - microenvironment
OT  - natural killer cells
OT  - tumor
EDAT- 2016/10/19 06:00
MHDA- 2018/01/18 06:00
CRDT- 2016/09/24 06:00
PHST- 2016/08/30 00:00 [received]
PHST- 2016/08/30 00:00 [accepted]
PHST- 2016/10/19 06:00 [pubmed]
PHST- 2018/01/18 06:00 [medline]
PHST- 2016/09/24 06:00 [entrez]
AID - 10.1111/tan.12898 [doi]
PST - ppublish
SO  - HLA. 2016 Nov;88(5):213-220. doi: 10.1111/tan.12898. Epub 2016 Sep 22.