Study on the Quantities and Functions of Natural Killer Cell Subsets in Peripheral Blood of the Patients with Severe Aplastic Anemia,

To investigate the quantitative and functional changes of natural killer(NK) cell subsets in peripheral blood of severe aplastic anemia(SAA) patients before and after immunosuppressive therapy(IST). Methods By means of monoclonal antibody labeling technology, the percentages of NK cells (CD3⁻CD56⁺ MCD16⁺) and their subsets[CD3⁻CD56^bright(CD56^bright),CD3⁻CD56^dim(CD56^dim),CD3⁻CD56⁻ CD16⁺)] in peripheral blood lymphocytes were detected in 42 SAA patients, including 12 patients with newly diagnosed SAA and 30 recovery patients, and 13 normal controls respectively. NK cells inhibitory receptors(CD158a and CD158b),activating receptors(NKG2D and NKp46), perforin and granzyme-β were also detected. Results The percentage of NK cells in peripheral blood lymphocytes was(10.30±6.08)% newly diagnosed patients,(16.47±8.29)% in recovery patients, and(19.45±6.88)% in normal controls. The percentage of NK cells in newly diagnosed SAA patients was lower than that of recovery patients and normal controls(p<0.05),and there was no statistical difference between recovery patients and normal controls(p>0.05).The median percentage of CD56^bright cells was 0.11% newly diagnosed SAA patients, 0.68% in recovery patients and 0.53% in normal controls. The median percentage of CD56^bright cells in newly diagnosed SAA patients was lower than that of the other two groups (p<0.05),and there was no statistical difference between recovery patients and normal controls(p>0.05).The percentage of CD56^dim cells was(9.62±6.04)% in newly diagnosed patients,(13.81±7.52)% in recovery patients and(18.21±7.16)% in normal controls. The percentage of CD56^dim cells in newly diagnosed SAA patients was lower than that of normal controls (p<0.05),and there was no statistical difference between the other groups(p>0.05).The median percentage of CD3⁻CD56⁻CD16⁺ cells was 0.37% in newly diagnosed patients, 0.79% in recovery patients and 0.41% in normal controls. The percentage of CD3⁻CD56⁻CD16⁺ cells in recovery SAA patients was higher than that of the other two groups(p<0.05),and there was no statistical difference between newly diagnosed SAA patients and normal controls (p>0.05).The median expressions of CD158a,NKG2D and NKp46 on NK cells were 16.45%,95.68%,88.23% in newly diagnosed SAA patients, 19.34%,96.85%,82.97% in recovery patients and 21.59%,96.13%,40.99% in normal controls. The median expression of NKp46 on NK cells of newly diagnosed and recovery SAA patients were higher than that of healthy individuals(p<0.05).The expression of CD158b on NK cells was(34.66±16.02)% in newly diagnosed patients,(39.13±17.75)% in recovery patients,(41.43±17.43)% in controls, and there was no statistical difference between each groups (p>0.05).The expression of perforin in NK cells cytoplasm was(66.14±20.73)% in newly diagnosed patients,(64.97±21.61)% in recovery patients and (42.11±_27.25)% in controls. The expression of perforin in newly diagnosed and recovery SAA patients were higher than that of controls(p<0.05),and there was no statistical difference between that of the other groups (p>0.05).The median expression of granzyme-β in NK cells cytoplasm is 96.43% in newly diagnosed SAA patients,96.97% in recovery SAA patients,92.88% in controls, and there was no statistical difference between each groups (p>0.05). Conclusions The decrease of the percentage NK cells, CD56^bright,CD56^dim NK cell subsets and the higher expressions of NKp46 and perforin may cause the over-function of T lymphocytes and thus lead to hematopoiesis failure in SAA≤®.

No relevant conflicts of interest to declare.