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

doi:10.1186/1471-2164-7-263

BMC Genomics

Volume 7

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Franzke A
Geffers R
Hunger JK
Pförtner S
Piao W
Ivanyi P
Grosse J
Probst-Kepper M
Ganser A
Buer J

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Franzke A
Geffers R
Hunger JK
Pförtner S
Piao W
Ivanyi P
Grosse J
Probst-Kepper M
Ganser A
Buer J
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Research article

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

Anke Franzke¹ , Robert Geffers² , J Katrin Hunger¹ , Susanne Pförtner² , Wenji Piao¹ , Philipp Ivanyi¹ , Jens Grosse¹ , Michael Probst-Kepper⁴ , Arnold Ganser¹ and Jan Buer²^,3

¹Department of Hematology, Hemostasis and Oncology, Hannover Medical School, Carl-Neuberg-Str.1, D-30625 Hannover, Germany

²Department of Cell Biology and Immunology, Helmholtz Centre for Infection Research, Inhoffenstraße 7, D-38124 Braunschweig, Germany

³Department of Medical Microbiology, Hannover Medical School, Carl-Neuberg-Str.1, D-30625 Hannover, Germany

⁴Junior Research Group for Xenotransplantation, Department of Visceral and Transplant Surgery, Hannover Medical School, Carl-Neuberg-Str.1, D-30625 Hannover, Germany

author email corresponding author email

BMC Genomics 2006, 7:263doi:10.1186/1471-2164-7-263


Published:	19 October 2006

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.