Tumor-induced tolerance and immune suppression by myeloid derived suppressor cells

Emerging evidence indicates that the Achilles' heel of cancer immunotherapies is often the complex interplay of tumor-derived factors and deviant host properties, which involve a wide range of immune elements in the lymphoid and myeloid compartments. Regulatory lymphocytes, tumor-conditioned my...

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Bibliographic Details
Published in:Immunological reviews 2008-04, Vol.222 (1), p.162-179
Main Authors: Marigo, Ilaria, Dolcetti, Luigi, Serafini, Paolo, Zanovello, Paola, Bronte, Vincenzo
Format: Article
Language:English
Subjects:
Animals
Antigens, CD34 - immunology
arginine metabolism
cancer
CD11 Antigens - immunology
CD8-Positive T-Lymphocytes - immunology
Cell Communication
Down-Regulation
Granulocyte-Macrophage Colony-Stimulating Factor - immunology
Immune Tolerance
Immunosuppression
Interleukin-4 Receptor alpha Subunit - immunology
Lymphocyte Activation
MDSC
Mice
Models, Immunological
Myeloid Cells - immunology
Myelopoiesis - immunology
neoplasms
Neoplasms - immunology
Neoplasms - pathology
Nitric Oxide Synthase Type II - immunology
Signal Transduction - immunology
T-Lymphocytes, Regulatory - immunology
tolerance
Tumor Escape
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Summary:Emerging evidence indicates that the Achilles' heel of cancer immunotherapies is often the complex interplay of tumor-derived factors and deviant host properties, which involve a wide range of immune elements in the lymphoid and myeloid compartments. Regulatory lymphocytes, tumor-conditioned myeloid-derived suppressor cells (MDSCs), tumor-associated macrophages, and dysfunctional and immature dendritic cells take part in a complex immunoregulatory network. Despite the fact that some mechanisms governing tumor-induced immune tolerance and suppression are starting to be better understood and their complexity dissected, little is known about the diachronic picture of immune tolerance. Based on observations of MDSCs, we present a time-structured and topologically consistent idea of tumor-dependent tolerance progression in tumor-bearing hosts.
ISSN:0105-2896
1600-065X
DOI:10.1111/j.1600-065X.2008.00602.x