[Changes of natural kill cell in peripheral blood of patients with myelodysplastic syndrome].
OBJECTIVE
To analyze the percentage and functional changes of natural kill (NK) cell in peripheral blood of myelodysplastic syndrome (MDS) patients so as to evaluate the relationships between these changes and hematopoietic functions and explore the role of NK cell in the pathogenesis of MDS.


METHODS
By flow cytometry, the percentage of NK cell (CD3⁻CD56⁺CD16⁺) in peripheral blood lymphocytes was detected in 20 MDS patients, 15 acute myelogenous leukemic (AML) and 15 normal controls from March 2013 to November 2013 at our hospital.NK cell activation receptors (NKG2D, NKp44), inhibitory receptors (CD158a, CD158b), perforin and granzyme-β of patients and normal controls were also detected. The correlation between these changes and hematopoietic functions, including the percentages of neutrophil granulocyte (ANC%), lymphocyte (Lym%), reticulocyte (RET%) and hemoglobin, thrombocyte in peripheral blood and the hematopoietic function in bone marrow (CD34⁺%) were evaluated.


RESULTS
(1) The percentage of NK cell (3.87% ± 0.97%) in MDS patients was significantly lower than that of normal controls (6.08% ± 1.37%, P < 0.05) and higher than that of AML patients (2.58% ± 0.78%, P < 0.05).(2) The expression of NKG2D in MDS patients (52.83%) was significantly lower than that of normal controls (86.36%, P < 0.05) and higher than that of AML patients (42.00%, P < 0.05). The expression of NKp44 in MDS patients (2.41%) was significantly higher than that of normal controls (0.62%) and AML patients (0.92%) (both P < 0.05). (3) The expression of CD158a in MDS and AML patients (5.46% ± 2.40%, 4.05% ± 1.89%) were significantly both lower than those of normal controls (7.97% ± 2.85%, both P < 0.05). The expression of CD158b had no significant difference among the 3 groups. (4) The expression of perforin in MDS patients (17.83%) was significantly lower than that of normal controls (59.79%, P < 0.05) and higher than that of AML patients (13.06%, P < 0.05). The expressions of granzyme-β in MDS and AML patients (21.54%, 30.65%) were significantly both lower than those of normal controls (83.42%, both P < 0.05). (5) The percentage of NK cell and the expression of NKG2D and NKp44 in MDS patients with low-risk group were in turn higher than those of high-risk group (4.06% ± 0.56% vs 3.59% ± 1.37%, 53.42% ± 6.85% vs 47.29% ± 8.08%, 2.46% vs 2.07%, all P < 0.05) , the expression of CD158a and CD158b were in turn lower than those of high-risk group, but both P > 0.05.(6) The percentage of NK was positively correlated with ANC% (r = 0.780, P < 0.05), but negatively with Lym% and the CD34⁺% in bone marrow (r = -0.543, -0.610, both P < 0.05). The expression of CD158a was positively correlated with CD34⁺% in bone marrow (r = 0.612, P < 0.05). The expressions of NKp44, CD158a, perforin and granzyme-β of NK cells had no correlation with hematopoiesis (all P > 0.05).


CONCLUSIONS
The lowered percentage and function of NK may cause the immunological dysfunction and lead to underkill of pathological hematopoietic cells in MDS.
Department of Hematology, General Hospital, Tianjin Medical University, Tianjin 300052, China.
Huijing
H
Mi
Department of Hematology, General Hospital, Tianjin Medical University, Tianjin 300052, China.
Rong
R
Fu
Department of Hematology, General Hospital, Tianjin Medical University, Tianjin 300052, China.
Huaquan
H
Wang
Department of Hematology, General Hospital, Tianjin Medical University, Tianjin 300052, China.
Wen
W
Qu
Department of Hematology, General Hospital, Tianjin Medical University, Tianjin 300052, China.
Erbao
E
Ruan
Department of Hematology, General Hospital, Tianjin Medical University, Tianjin 300052, China.
Xiaoming
X
Wang
Department of Hematology, General Hospital, Tianjin Medical University, Tianjin 300052, China.
Guojin
G
Wang
Department of Hematology, General Hospital, Tianjin Medical University, Tianjin 300052, China.
Hong
H
Liu
Department of Hematology, General Hospital, Tianjin Medical University, Tianjin 300052, China.
Yuhong
Y
Wu
Department of Hematology, General Hospital, Tianjin Medical University, Tianjin 300052, China.
Jia
J
Song
Department of Hematology, General Hospital, Tianjin Medical University, Tianjin 300052, China.
Limin
L
Xing
Department of Hematology, General Hospital, Tianjin Medical University, Tianjin 300052, China.
Jing
J
Guan
Department of Hematology, General Hospital, Tianjin Medical University, Tianjin 300052, China.
Lijuan
L
Li
Department of Hematology, General Hospital, Tianjin Medical University, Tianjin 300052, China.
Huijuan
H
Jiang
Department of Hematology, General Hospital, Tianjin Medical University, Tianjin 300052, China.
Wei
W
Zhang
Department of Hematology, General Hospital, Tianjin Medical University, Tianjin 300052, China.
Lanzhu
L
Yue
Department of Hematology, General Hospital, Tianjin Medical University, Tianjin 300052, China. Email: shaozonghong@sina.com.
Zonghong
Z
Shao
D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D016022:Case-Control Studies; D005260:Female; D053804:Granzymes / Q000378:metabolism; D006801:Humans; D007694:Killer Cells, Natural / Q000276:immunology* / Q000378:metabolism*; D015470:Leukemia, Myeloid, Acute; D008297:Male; D008875:Middle Aged; D009190:Myelodysplastic Syndromes / Q000097:blood* / Q000276:immunology*; D055655:NK Cell Lectin-Like Receptor Subfamily K / Q000378:metabolism; D055629:Natural Cytotoxicity Triggering Receptor 2 / Q000378:metabolism; D054353:Perforin / Q000378:metabolism; D054344:Receptors, KIR2DL3 / Q000378:metabolism; D055815:Young Adult
C527085:KLRK1 protein, human; C112837:NCR2 protein, human; D055655:NK Cell Lectin-Like Receptor Subfamily K; D055629:Natural Cytotoxicity Triggering Receptor 2; D054344:Receptors, KIR2DL3; D054353:Perforin; D053804:Granzymes