Abstract
Myelodysplastic syndromes (MDS) are heterogeneous clonal hematologic malignancies characterized by cytopenias caused by ineffective hematopoiesis and propensity to progress to acute myeloid leukemia. Innate immunity provides immediate protection against pathogens by coordinating activation of signaling pathways in immune cells. Given the prominent role of the innate immune pathway in regulating hematopoiesis, it is not surprising that aberrant signaling of this pathway is associated with hematologic malignancies. Increased activation of the innate immune pathway may contribute to dysregulated hematopoiesis, dysplasia, and clonal expansion in myelodysplastic syndromes.
Copyright (c) 2010 Elsevier Inc. All rights reserved.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Cell Transformation, Neoplastic / genetics
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Cytokines / biosynthesis
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Cytokines / genetics
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Gene Expression Regulation / immunology
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Genes, MHC Class II
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Hematopoiesis / immunology
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Hematopoietic Stem Cells / cytology
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Hematopoietic Stem Cells / immunology
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Humans
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Immunity, Innate* / genetics
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Inflammation / immunology
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Leukemia, Myeloid, Acute / genetics
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Leukemia, Myeloid, Acute / immunology
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Mice
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MicroRNAs / genetics
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Myelodysplastic Syndromes / genetics
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Myelodysplastic Syndromes / immunology*
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Receptors, Immunologic / immunology
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Receptors, Tumor Necrosis Factor / immunology
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Toll-Like Receptors / immunology
Substances
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Cytokines
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MicroRNAs
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Receptors, Immunologic
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Receptors, Tumor Necrosis Factor
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Toll-Like Receptors