The shortening telomere length of T lymphocytes maybe associated with hyper‑function in servere aplastic anemia.

Severe aplastic anemia (SAA) is a primary disorder of severe bone marrow failure characterizing with extreme pancytopenia and a profound diminution of bone marrow progenitor cells, which is associated with T cell hyper‑function. Abnormal telomere shortening of bone marrow mononuclear cell has been reported in AA, which may lead to genomic instability, and result in cell senescence or apoptosis. Notably, certain studies identfieid that lymphocytes of shortening telomere length have undergone apoptosis escape in autoimmune diseases. In order to investigate the association between telomere lengths and function of T lymphocytes in SAA, the relative telomere lengths (RTLs) of different subtypes of T lymphocytes were investigated by flow‑fluorescent in situ hybridization in 30 patients with SAA and 25 healthy controls. Then the levels of expression of cluster of differentiation 28 (CD28), CD158 and CD70 were measured, which represent the function of T lymphocytes. The apoptosis rate and the cell cycle progression of CD8+T lymphocytes, and the level of secretion interferon‑γ and tumor necrosis factor‑α were also measured. Finally, the correlation between telomere length and these functional events of CD8+T lymphocytes was analyzed in patients with SAA. The results showed that RTLs of CD8+T lymphocytes in SAA were significantly shorter compared with those in controls. Furthermore, in patients with SAA, CD8+T lymphocytes are associated with T cell hyper‑function, which is related to the RTL. Thus, the shorter RTLs of CD8+T lymphocytes in SAA may be associated with hyper‑function of these cells, which contribute to the pathogenesis of SAA.