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Review
. 2010 Jan;17(1):6-10.
doi: 10.1016/j.jocn.2009.05.006. Epub 2009 Nov 18.

The role of microglia in central nervous system immunity and glioma immunology

Affiliations
Review

The role of microglia in central nervous system immunity and glioma immunology

Isaac Yang et al. J Clin Neurosci. 2010 Jan.

Abstract

The central nervous system (CNS) historically has been considered an immune-privileged organ, lacking a lymphatic system and shielded from the circulatory system by the blood-brain barrier. Microglia are an abundant portion of the CNS cell population, comprising 5% to 20% of the total glial cell population, and are as numerous as neurons. A crucial function of microglia is the ability to generate significant innate and adaptive immune responses. Microglia are involved in first line innate immunity of the CNS. Proper antigen presentation is critical in the generation of specific, durable responses by the adaptive immune system, and requires interaction between the T cell receptor and processed antigen peptide presented on major histocompatibility complex (MHC) molecules by the antigen presenting cells (APC). Microglia also have a large regulatory role in CNS immunity. Histopathologic studies of glioma tissue have consistently shown high levels of infiltrating microglia. Microglia are also localized diffusely throughout the tumor, rather than to the areas of necrosis, and phagocytosis of glioma cells or debris by microglia is not observed. Recent evidence indicates that glioma-infiltrating microglia/macrophages might be promoting tumor growth by facilitating immunosuppression of the tumor microenvironment. When activated, microglia can be potent immune effector cells, able to perform a broad range of functions, and they mediate both innate and adaptive responses during CNS injury and disease while remaining quiescent in the steady state. Their versatility in bridging the gap between the immune-privileged CNS and the peripheral immune system, in addition to their significant numbers in gliomas, makes them an attractive candidate in immunotherapy for gliomas. An enhanced understanding of microglia-glioma interaction may provide better methods to manipulate the glioma microenvironment to allow the generation of a specific and durable anti-glioma immunity. The role of microglia in CNS immunity is reviewed, with a focus on key advances made in glioma immunology.

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References

    1. Hao C, I, Parney F, Roa WH, et al. Cytokine and cytokine receptor mRNA expression in human glioblastomas: evidence of Th1, Th2 and Th3 cytokine dysregulation. Acta Neuropathol (Berl) 2002;103(2):171–8. - PubMed
    1. Badie B, Schartner JM, Paul J, et al. Dexamethasone-induced abolition of the inflammatory response in an experimental glioma model: a flow cytometry study. J Neurosurg. 2000;93(4):634–9. - PubMed
    1. Yang I, Kremen TJ, Giovannone AJ, et al. Modulation of major histocompatibility complex Class I molecules and major histocompatibility complex-bound immunogenic peptides induced by interferon-alpha and interferon-gamma treatment of human glioblastoma multiforme. J Neurosurg. 2004;100(2):310–9. - PubMed
    1. Aloisi F, De Simone R, Columba-Cabezas S, et al. Functional maturation of adult mouse resting microglia into an APC is promoted by granulocyte-macrophage colony-stimulating factor and interaction with Th1 cells. J Immunol. 2000;164(4):1705–12. - PubMed
    1. Ayoub AE, Salm AK. Increased morphological diversity of microglia in the activated hypothalamic supraoptic nucleus. J Neurosci. 2003;23(21):7759–66. - PMC - PubMed

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