Abstract
The central nervous system (CNS) is characterized by unique immune biology. Distinct mechanisms of CNS immune surveillance and activation have important implications in tumor development as CNS tumors are known to evade anti-tumoral immunity, and may also contribute to immunosuppression. Multiple cell-surface and secreted mediators, expressed in both CNS tumor cells and responding immune cells, have been shown to influence the immune response to CNS tumors. In this review we provide an overview of CNS tumor immune escape and immunosuppression, highlighting the cellular and molecular features associated with both CNS tumors cells and responding immune cells. In this context, we discuss of the role of the M1 and M2 tumor associated macrophage phenotypes, myeloid derived suppressor cells, regulatory T-cells, as well as many immunomodulatory cytokines. Additionally, recent insights into the STAT-3 intracellular signaling pathway and the presence of active human CMV infection in the context of CNS tumor development are discussed.
Highlights
Cancers of the central nervous system (CNS) are unique in their interaction with the immune system throughout development and progression
The CNS was long viewed as an “immune-privileged” site due to a perceived lack of antigen presenting cells (APCs), restriction from circulating lymphocytes and other immune mediators by the blood brain barrier (BBB), and absence of lymphatic drainage
Immune competence is dependent upon the activation of resident microglia and infiltrating macrophages capable of effective lymphocyte activation, all permissible through inducible permeability of the BBB to immune mediators [6,13]
Summary
Received Date: March 12, 2014; Accepted Date: April 26, 2014; Published Date: May 5, 2014
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