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CD200 expression suppresses natural killer cell function and directly inhibits patient anti-tumor response in acute myeloid leukemia.

Abstract：

:Upregulation of the immunosuppressive cell surface glycoprotein, CD200, is a common feature of acute myeloid leukemia (AML) and is associated with poor patient outcome. We investigated whether CD200 overexpression on AML cells could specifically compromise patient natural killer (NK) cell anti-tumor responses. We found that CD200(hi) patients showed a 50% reduction in the frequency of activated NK cells (CD56(dim)CD16(+)) compared with CD200(lo) patients. Additionally, NK receptor expression (NKp44 and NKp46) on these cells was also significantly downregulated in CD200(hi) patients. To assess whether NK cell activity was directly influenced by CD200 expression, we examined the effect of ectopic expression of CD200. These assays revealed that both NK cell cytolytic activity and interferon-γ response were significantly reduced toward CD200(+) leukemic targets and that these targets showed increased survival compared with CD200(-) cells. Similarly, NK cells isolated from AML patients were less functionally active toward CD200(hi) autologous blasts from both cytolytic and immunoregulatory perspectives. Finally, blocking CD200 alone was sufficient to recover a significant proportion of NK cell cytolytic activity. Together, these findings provide the first evidence that CD200 has a direct and significant suppressive influence on NK cell activity in AML patients and may contribute to the increased relapse rate in CD200(+) patients.

journal_name

Leukemia

journal_title

Leukemia

authors

Coles SJ,Wang EC,Man S,Hills RK,Burnett AK,Tonks A,Darley RL

doi

10.1038/leu.2011.1

subject

Has Abstract

pub_date

2011-05-01 00:00:00

pages

792-9

issue

5

eissn

0887-6924

issn

1476-5551

pii

leu20111

journal_volume

25

pub_type

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