Type I natural killer T cells suppress tumors caused by p53 loss in mice

被引：77

作者：

Swann, Jeremy B. ^{[1
,2
]}

Uldrich, Adam P. ^{[1
]}

van Dommelen, Serani ^{[1
]}

Sharkey, Janelle ^{[1
]}

Murray, William K. ^{[4
]}

Godfrey, Dale I. ^{[3
]}

Smyth, Mark J. ^{[1
,2
]}

机构：

[1] Peter MacCallum Canc Ctr, Canc Immunol Program, Sir Donald & Lady Trescowthick Labs, Melbourne, Vic, Australia

[2] Univ Melbourne, Dept Pathol, Parkville, Vic 3052, Australia

[3] Univ Melbourne, Dept Microbiol & Immunol, Parkville, Vic 3052, Australia

[4] Peter MacCallum Canc Ctr, Dept Pathol, Melbourne, Vic, Australia

来源：

BLOOD | 2009年 / 113卷 / 25期

基金：

美国国家卫生研究院; 英国医学研究理事会;

关键词：

NKT CELLS; ALPHA-GALACTOSYLCERAMIDE; IMMUNOSURVEILLANCE; SURVEILLANCE; LYMPHOMA; CANCER; MUTATIONS; IMMUNITY; SARCOMAS; HOSTS;

D O I：

10.1182/blood-2009-01-198564

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

CD1d-restricted T cells are considered to play a host protective effect in tumor immunity, yet the evidence for a role of natural killer T (NKT) cells in tumor immune surveillance has been weak and data from several tumor models has suggested that some (type II) CD1d-restricted T cells may also suppress some types of antitumor immune response. To substantiate an important role for CD1d-restricted T cells in host response to cancer, we have evaluated tumor development in p53(+/-) mice lacking either type I NKT cells (TCR J alpha 18(-/-)) or all CD1d-restricted T cells (CD1d(-/-)). Our findings support a key role for type I NKT cells in suppressing the onset of sarcomas and hematopoietic cancers caused by p53 loss but do not suggest that other CD1d-restricted T cells are critical in regulating the same tumor development. (Blood. 2009; 113: 6382-6385)

引用

页码：6382 / 6385

页数：4

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