Expression of interferon consensus sequence binding protein induces potent immunity against BCR/ABL-induced leukemia

被引：48

作者：

Deng, M

Daley, GQ

机构：

[1] Whitehead Inst, Cambridge, MA 02142 USA

[2] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Hematol Oncol, Boston, MA USA

来源：

BLOOD | 2001年 / 97卷 / 11期

关键词：

D O I：

10.1182/blood.V97.11.3491

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Mice deficient in the interferon consensus sequence binding protein (ICSBP) develop a disease resembling chronic myeloid leukemia (CML), which in humans is caused by the BCR/ABL oncoprotein. Interferon-alpha (IFN-alpha) induces ICSBP expression and is an effective therapy for CML, This study examined whether enforced expression of ICSBP might antagonize BCR/ABL-induced leukemia; results demonstrated that ICSBP-modified cells generated a protective CD8(+) cytotoxic T-cell response against BCR/ABL-transformed BaF3 cells in a murine leukemia model. ICSBP expression represents a novel means of stimulating a host immune response to BCR/ABL(+) leukemia cells and a potential strategy for immunotherapy of CML. (Blood, 2001;97:3491-3497) (C) 2001 by The American Society of Hematology.

引用

收藏

页码：3491 / 3497

页数：7

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