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The immunoregulatory mechanisms of carcinoma for its survival and development

The immune system in patients detects and eliminates tumor cells, but tumors still progress persistently. The mechanisms by which tumor cells survive under the pressure of immune surveillance are not fully understood. This review is to present the evidence from clinical studies, showing a significan...

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Detalles Bibliográficos
Autores principales: Du, Caigan, Wang, Yuzhuo
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3031251/
https://www.ncbi.nlm.nih.gov/pubmed/21255410
http://dx.doi.org/10.1186/1756-9966-30-12
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author Du, Caigan
Wang, Yuzhuo
author_facet Du, Caigan
Wang, Yuzhuo
author_sort Du, Caigan
collection PubMed
description The immune system in patients detects and eliminates tumor cells, but tumors still progress persistently. The mechanisms by which tumor cells survive under the pressure of immune surveillance are not fully understood. This review is to present the evidence from clinical studies, showing a significant correlation of clinicopathological features of carcinoma with: (1) the loss of classical human leukocyte antigen class I, (2) the up-regulation of non-classical human leukocyte antigen class I, pro-apoptotic Fas ligand and receptor-binding cancer antigen expressed on SiSo cells I, and (3) the formation of immunosuppressive microenvironment by up-regulation of transforming growth factor-beta, Galectin-1, inhibitory ligand B7s, indoleamine 2,3-dioxygenase and arginase, as well as by recruitment of tumor-induced myeloid-derived suppressor cells and regulatory T cells. All of these factors may together protect carcinoma cells from the immune-cytotoxicity.
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spelling pubmed-30312512011-02-01 The immunoregulatory mechanisms of carcinoma for its survival and development Du, Caigan Wang, Yuzhuo J Exp Clin Cancer Res Review The immune system in patients detects and eliminates tumor cells, but tumors still progress persistently. The mechanisms by which tumor cells survive under the pressure of immune surveillance are not fully understood. This review is to present the evidence from clinical studies, showing a significant correlation of clinicopathological features of carcinoma with: (1) the loss of classical human leukocyte antigen class I, (2) the up-regulation of non-classical human leukocyte antigen class I, pro-apoptotic Fas ligand and receptor-binding cancer antigen expressed on SiSo cells I, and (3) the formation of immunosuppressive microenvironment by up-regulation of transforming growth factor-beta, Galectin-1, inhibitory ligand B7s, indoleamine 2,3-dioxygenase and arginase, as well as by recruitment of tumor-induced myeloid-derived suppressor cells and regulatory T cells. All of these factors may together protect carcinoma cells from the immune-cytotoxicity. BioMed Central 2011-01-21 /pmc/articles/PMC3031251/ /pubmed/21255410 http://dx.doi.org/10.1186/1756-9966-30-12 Text en Copyright ©2011 Du and Wang; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review
Du, Caigan
Wang, Yuzhuo
The immunoregulatory mechanisms of carcinoma for its survival and development
title The immunoregulatory mechanisms of carcinoma for its survival and development
title_full The immunoregulatory mechanisms of carcinoma for its survival and development
title_fullStr The immunoregulatory mechanisms of carcinoma for its survival and development
title_full_unstemmed The immunoregulatory mechanisms of carcinoma for its survival and development
title_short The immunoregulatory mechanisms of carcinoma for its survival and development
title_sort immunoregulatory mechanisms of carcinoma for its survival and development
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3031251/
https://www.ncbi.nlm.nih.gov/pubmed/21255410
http://dx.doi.org/10.1186/1756-9966-30-12
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