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

Abstract

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)

• Authors: M Deng, G Q Daley
• Journal: Blood (Blood) Vol. 97 Issue 11 Pg. 3491-7 (Jun 01 2001) ISSN: 0006-4971 [Print] United States
• PMID: 11369642 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)

Chemical References

• Interferon Regulatory Factors
• Repressor Proteins
• interferon regulatory factor-8
• Interferons
• Fusion Proteins, bcr-abl

Topics

• Animals
• CD8-Positive T-Lymphocytes (immunology)
• Cell Transformation, Neoplastic
• Female
• Fusion Proteins, bcr-abl (analysis, genetics, physiology)
• Gene Expression
• Immunity
• Immunization
• Interferon Regulatory Factors
• Interferons (physiology)
• Leukemia (immunology, prevention & control)
• Mice
• Mice, Inbred BALB C
• Mice, Inbred NOD
• Mice, SCID
• Neoplasm Transplantation
• Repressor Proteins (genetics, physiology)
• Reverse Transcriptase Polymerase Chain Reaction
• Spleen (immunology)
• Transfection