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dc.contributor.authorJohnson, Theodore S.
dc.contributor.authorMunn, David H.
dc.contributor.authorMaria, Bernard L.
dc.date.accessioned2012-10-26T20:30:42Z
dc.date.available2012-10-26T20:30:42Z
dc.date.issued2012-01-24en_US
dc.identifier.citationClin Dev Immunol. 2012 Jan 24; 2012:937253en_US
dc.identifier.issn1740-2530en_US
dc.identifier.pmid22312408en_US
dc.identifier.doi10.1155/2012/937253en_US
dc.identifier.urihttp://hdl.handle.net/10675.2/776
dc.description.abstractCentral nervous system tumors take advantage of the unique immunology of the CNS and develop exquisitely complex stromal networks that promote growth despite the presence of antigen-presenting cells and tumor-infiltrating lymphocytes. It is precisely this immunological paradox that is essential to the survival of the tumor. We review the evidence for functional CNS immune privilege and the impact it has on tumor tolerance. In this paper, we place an emphasis on the role of tumor-infiltrating myeloid cells in maintaining stromal and vascular quiescence, and we underscore the importance of indoleamine 2,3-dioxygenase activity as a myeloid-driven tumor tolerance mechanism. Much remains to be discovered regarding the tolerogenic mechanisms by which CNS tumors avoid immune clearance. Thus, it is an open question whether tumor tolerance in the brain is fundamentally different from that of peripheral sites of tumorigenesis or whether it simply stands as a particularly strong example of such tolerance.
dc.rightsCopyright © 2012 Theodore S. Johnson et al.en_US
dc.subjectReview Articleen_US
dc.titleModulation of Tumor Tolerance in Primary Central Nervous System Malignanciesen_US
dc.typeArticleen_US
dc.identifier.pmcidPMC3270544en_US
dc.contributor.corporatenameDepartment of Pediatrics
dc.contributor.corporatenameImmunotherapy Center
dc.contributor.corporatenameGHSU Cancer Center
refterms.dateFOA2019-04-10T00:49:44Z
html.description.abstractCentral nervous system tumors take advantage of the unique immunology of the CNS and develop exquisitely complex stromal networks that promote growth despite the presence of antigen-presenting cells and tumor-infiltrating lymphocytes. It is precisely this immunological paradox that is essential to the survival of the tumor. We review the evidence for functional CNS immune privilege and the impact it has on tumor tolerance. In this paper, we place an emphasis on the role of tumor-infiltrating myeloid cells in maintaining stromal and vascular quiescence, and we underscore the importance of indoleamine 2,3-dioxygenase activity as a myeloid-driven tumor tolerance mechanism. Much remains to be discovered regarding the tolerogenic mechanisms by which CNS tumors avoid immune clearance. Thus, it is an open question whether tumor tolerance in the brain is fundamentally different from that of peripheral sites of tumorigenesis or whether it simply stands as a particularly strong example of such tolerance.


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