Aplastic anemia (AA) is a primary disorder of severe bone marrow failure characterized by pancytopenia. The pathogenesis of AA is closely related to T cell hyperfunction. Abnormal telomere shortening of bone marrow mononuclear cells which has been reported in AA not only lead to genomic instability and apoptosis but also regulate T cells immunity to antigen. Interestingly,lymphocytes with shorter telomere length have undergone apoptosis escape in autoimmune disease. In our study, the relative telomere length (RTLs) of CD3+, CD3+CD4+, CD3+CD8+, CD19+ and CD34+ cells were investigated in 14 untreated AA patients and 32 controls. The RTLs of CD3+,CD3+CD4+ and CD3+CD8+T lymphocytes were shorter than those of the controls. Meanwhile, no differences in CD19+B and CD34+ cells were found between AA and controls. A change in telomere length may be involved in the pathogenesis of AA and could be considered as a predictive biomarker for the diagnose of AA.

Disclosures

No relevant conflicts of interest to declare.

Author notes

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Asterisk with author names denotes non-ASH members.

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