Identification of novel regulators in T-cell differentiation of aplastic anemia patients.
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Authors
Franzke, AnkeGeffers, 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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Show full item recordAbstract
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, 7:263PubMed ID
17052335Type
ArticleLanguage
enISSN
1471-2164ae974a485f413a2113503eed53cd6c53
10.1186/1471-2164-7-263
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