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-α (IFN-α) 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.
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Forced expression of ICSBP induces potent immunity against Bcr-Abl-induced leukemia in mice, and in vivo leukemia caused by transformed BaF3 cells was completely inhibited by coexpression of ICSBP.
“Furthermore, it was shown that forced expression of ICSBP induces potent immunity against Bcr-Abl-induced leukemia in mice. (53)”
From Review: ICSBP/IRF-8: Its Regulatory Roles in the Development of Myeloid Cells (2002) · cites this paper as [53]
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The IRF Family Transcription Factors in Immunity and Oncogenesis
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Review: ICSBP/IRF-8: Its Regulatory Roles in the Development of Myeloid Cells
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- Authors
- Deng, M., & Daley, G. Q.
- Affiliations
- Harvard University (US)
- ORCID
- Daley, George Q.
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2001-06-01
- Volume
- 97
- Issue
- 11
- Pages
- 3491-3497
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- OpenAlex
- W1994905417
- Cited by
- 50
- References
- 47
- Citations by year
- 2025: 1 · 2022: 1 · 2021: 2 · 2017: 1 · 2016: 1 · 2015: 2 · 2014: 4 · 2013: 2 · 2012: 4
- FWCI
- 2.07
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Blood (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r29ca076418-04)
- National Cancer Institute (R01CA086991, CA 76418, CA86991)
- Topics
- Health Sciences › Medicine › Hematology › Chronic Myeloid Leukemia Treatments
- Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and Retrovirus Studies
- Keywords
- IRF8, BCR-ABL, chronic myeloid leukemia, interferon-alpha, CD8+ cytotoxic T lymphocytes, antitumor immunity, leukemia immunotherapy, Ba/F3 cells, gene therapy
- MeSH terms
- Interferon Regulatory Factor-8, Animals, Cell Transformation, Neoplastic, Female, Immunity, Immunization, Interferons, Leukemia, Mice, Inbred BALB C, Neoplasm Transplantation, Repressor Proteins, Spleen, Transfection, Gene Expression, Fusion Proteins, bcr-abl, Mice, SCID, Mice, Inbred NOD, CD8-Positive T-Lymphocytes, Reverse Transcriptase Polymerase Chain Reaction, Interferon Regulatory Factors, Mice
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