Research Article

Fas/FasL in the immune pathogenesis of severe aplastic anemia

Published: May 30, 2014
Genet. Mol. Res. 13 (2) : 4083-4088 DOI: https://doi.org/10.4238/2014.May.30.3
Cite this Article:
C.Y. Liu, R. Fu, H.Q. Wang, L.J. Li, H. Liu, J. Guan, T. Wang, W.W. Qi, E.B. Ruan, W. Qu, G.J. Wang, H. Liu, Y.H. Wu, J. Song, L.M. Xing, Z.H. Shao (2014). Fas/FasL in the immune pathogenesis of severe aplastic anemia. Genet. Mol. Res. 13(2): 4083-4088. https://doi.org/10.4238/2014.May.30.3
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Abstract

Fas/FasL protein expression of bone marrow hematopoietic cells was investigated in severe aplastic anemia (SAA) patients. Fas expression was evaluated in CD34+, GlycoA+, CD33+, and CD14+ cells labeled with monoclonal antibodies in newly diagnosed and remission SAA patients along with normal controls. FasL expression was evaluated in CD8+ cells in the same manner. In CD34+ cells, Fas expression was significantly higher in the newly diagnosed SAA group (46.59 ± 27.60%) than the remission (6.12 ± 3.35%; P < 0.01) and control (8.89 ± 7.28%; P < 0.01) groups. In CD14+, CD33+, and GlycoA+ cells, Fas levels were significantly lower in the newly diagnosed SAA group (29.29 ± 9.23, 46.88 ± 14.30, and 15.15 ± 9.26%, respectively) than in the remission (47.23 ± 31.56, 67.22 ± 34.68, and 43.56 ± 26.85%, respectively; P < 0.05) and normal control (51.25 ± 38.36, 72.06 ± 39.88, 50.38 ± 39.88%, respectively; P < 0.05) groups. FasL expression of CD8+ cells was significantly higher in the newly diagnosed SAA group (89.53 ± 45.68%) than the remission (56.39 ± 27.94%; P < 0.01) and control (48.63 ± 27.38%; P <0.01) groups. No significant differences were observed between the remission and control groups. FasL expression in CD8+ T cells was significantly higher in newly diagnosed patients, and CD34+, CD33+, CD14+, and GlycoA+ cells all showed Fas antigen expression. The Fas/FasL pathway might play an important role in excessive hematopoietic cell apoptosis in SAA bone marrow. Furthermore, CD34+ cells are likely the main targets of SAA immune injury.

Fas/FasL protein expression of bone marrow hematopoietic cells was investigated in severe aplastic anemia (SAA) patients. Fas expression was evaluated in CD34+, GlycoA+, CD33+, and CD14+ cells labeled with monoclonal antibodies in newly diagnosed and remission SAA patients along with normal controls. FasL expression was evaluated in CD8+ cells in the same manner. In CD34+ cells, Fas expression was significantly higher in the newly diagnosed SAA group (46.59 ± 27.60%) than the remission (6.12 ± 3.35%; P +, CD33+, and GlycoA+ cells, Fas levels were significantly lower in the newly diagnosed SAA group (29.29 ± 9.23, 46.88 ± 14.30, and 15.15 ± 9.26%, respectively) than in the remission (47.23 ± 31.56, 67.22 ± 34.68, and 43.56 ± 26.85%, respectively; P + cells was significantly higher in the newly diagnosed SAA group (89.53 ± 45.68%) than the remission (56.39 ± 27.94%; P + T cells was significantly higher in newly diagnosed patients, and CD34+, CD33+, CD14+, and GlycoA+ cells all showed Fas antigen expression. The Fas/FasL pathway might play an important role in excessive hematopoietic cell apoptosis in SAA bone marrow. Furthermore, CD34+ cells are likely the main targets of SAA immune injury.