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    Identification of novel regulators in T-cell differentiation of aplastic anemia patients.

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    Authors
    Franzke, Anke
    Geffers, Robert
    Hunger, J Katrin
    Pförtner, Susanne
    Piao, Wenji
    Ivanyi, Philipp
    Grosse, Jens
    Probst-Kepper, Michael
    Ganser, Arnold
    Buer, Jan
    Issue Date
    2006
    
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    Abstract
    BACKGROUND: Aplastic anemia (AA) is a bone marrow failure syndrome mostly characterized by an immune-mediated destruction of marrow hematopoietic progenitor/stem cells. The resulting hypocellularity limits a detailed analysis of the cellular immune response. To overcome this technical problem we performed a microarray analysis of CD3+ T-cells derived from bone marrow aspirates and peripheral blood samples of newly diagnosed AA patients and healthy volunteers. Two AA patients were additionally analyzed after achieving a partial remission following immunosuppression. The regulation of selected candidate genes was confirmed by real-time RT-PCR. RESULTS: Among more than 22,200 transcripts, 583 genes were differentially expressed in the bone marrow of AA patients compared to healthy controls. Dysregulated genes are involved in T-cell mediated cytotoxicity, immune response of Th1 differentiated T-cells, and major regulators of immune function. In hematological remission the expression levels of several candidate genes tend to normalize, such as immune regulators and genes involved in proinflammatory immune response. CONCLUSION: Our study suggests a pivotal role of Th1/Tc1 differentiated T-cells in immune-mediated marrow destruction of AA patients. Most importantly, immune regulatory genes could be identified, which are likely involved in the recovery of hematopoiesis and may help to design new therapeutic strategies in bone marrow failure syndromes.
    Citation
    BMC Genomics 2006, 7:263
    URI
    http://hdl.handle.net/10033/12368
    DOI
    10.1186/1471-2164-7-263
    PubMed ID
    17052335
    Type
    Article
    Language
    en
    ISSN
    1471-2164
    ae974a485f413a2113503eed53cd6c53
    10.1186/1471-2164-7-263
    Scopus Count
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