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Article: Aberrant dendritic cell differentiation initiated by the Mll-Een fusion gene does not require leukemic transformation

TitleAberrant dendritic cell differentiation initiated by the Mll-Een fusion gene does not require leukemic transformation
Authors
KeywordsDevelopment
Myeloid leukemia
Issue Date2008
PublisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.jleukbio.org/
Citation
Journal Of Leukocyte Biology, 2008, v. 83 n. 1, p. 173-180 How to Cite?
AbstractDendritic cells (DCs), as specialized APCs, play a key role in the induction of anti-tumor immunity. They originate from bone marrow (BM) progenitors, which are frequently the targets of chromosomal translocations leading to development of leukemia. Aberrant DC differentiation and functions have been observed and are widely reported in patients with leukemia. It is not clear, however, whether such defects are a direct effect of a leukemic fusion gene or simply an outcome of the clinical disease. In this study, we demonstrate for the first time that knockin of the Mll-Een fusion gene can affect myeloid DC differentiation and functions directly, independent of the leukemic disease activities. We showed that the Mll-Een-expressing BM cells [enhanced green fluorescent protein+ (EGFP+)] from leukemic and nonleukemic mice had similarly impaired DC differentiation capacities with functional abnormalities. In contrast, BM cells without Mll-Een expression (EGFP-) showed normal DC differentiation and functions. A reduction in the frequency of CD11c+ DCs was also observed within the EGFP+ population in spleen and lymph nodes, and these cells were dysfunctional. Taken together, our findings suggest that the Mll-Een fusion gene can affect myeloid DC differentiation directly and functions in a cell-autonomous manner, where fully leukemic transformation of the hematopoietic progenitors is not required exclusively. Therefore, the study provides evidence for a direct causal relationship between leukemic gene fusion and abnormal DC differentiation, possibly contributing to the development of leukemia. © Society for Leukocyte Biology.
Persistent Identifierhttp://hdl.handle.net/10722/148538
ISSN
2023 Impact Factor: 3.6
2023 SCImago Journal Rankings: 1.521
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorSun, Qen_US
dc.contributor.authorKong, CTen_US
dc.contributor.authorHuang, FPen_US
dc.contributor.authorChan, LCen_US
dc.date.accessioned2012-05-29T06:13:35Z-
dc.date.available2012-05-29T06:13:35Z-
dc.date.issued2008en_US
dc.identifier.citationJournal Of Leukocyte Biology, 2008, v. 83 n. 1, p. 173-180en_US
dc.identifier.issn0741-5400en_US
dc.identifier.urihttp://hdl.handle.net/10722/148538-
dc.description.abstractDendritic cells (DCs), as specialized APCs, play a key role in the induction of anti-tumor immunity. They originate from bone marrow (BM) progenitors, which are frequently the targets of chromosomal translocations leading to development of leukemia. Aberrant DC differentiation and functions have been observed and are widely reported in patients with leukemia. It is not clear, however, whether such defects are a direct effect of a leukemic fusion gene or simply an outcome of the clinical disease. In this study, we demonstrate for the first time that knockin of the Mll-Een fusion gene can affect myeloid DC differentiation and functions directly, independent of the leukemic disease activities. We showed that the Mll-Een-expressing BM cells [enhanced green fluorescent protein+ (EGFP+)] from leukemic and nonleukemic mice had similarly impaired DC differentiation capacities with functional abnormalities. In contrast, BM cells without Mll-Een expression (EGFP-) showed normal DC differentiation and functions. A reduction in the frequency of CD11c+ DCs was also observed within the EGFP+ population in spleen and lymph nodes, and these cells were dysfunctional. Taken together, our findings suggest that the Mll-Een fusion gene can affect myeloid DC differentiation directly and functions in a cell-autonomous manner, where fully leukemic transformation of the hematopoietic progenitors is not required exclusively. Therefore, the study provides evidence for a direct causal relationship between leukemic gene fusion and abnormal DC differentiation, possibly contributing to the development of leukemia. © Society for Leukocyte Biology.en_US
dc.languageengen_US
dc.publisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.jleukbio.org/en_US
dc.relation.ispartofJournal of Leukocyte Biologyen_US
dc.subjectDevelopment-
dc.subjectMyeloid leukemia-
dc.subject.meshAnimalsen_US
dc.subject.meshCell Differentiation - Genetics - Immunologyen_US
dc.subject.meshCell Movement - Immunologyen_US
dc.subject.meshCell Transformation, Neoplastic - Genetics - Immunologyen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshCytokines - Biosynthesisen_US
dc.subject.meshDendritic Cells - Immunologyen_US
dc.subject.meshFlow Cytometry - Methodsen_US
dc.subject.meshLeukemia - Genetics - Immunologyen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Inbred C57blen_US
dc.subject.meshMyeloid-Lymphoid Leukemia Protein - Genetics - Metabolismen_US
dc.subject.meshT-Lymphocytes - Immunologyen_US
dc.titleAberrant dendritic cell differentiation initiated by the Mll-Een fusion gene does not require leukemic transformationen_US
dc.typeArticleen_US
dc.identifier.emailChan, LC:chanlc@hkucc.hku.hken_US
dc.identifier.authorityChan, LC=rp00373en_US
dc.description.naturelink_to_OA_fulltexten_US
dc.identifier.doi10.1189/jlb.0607348en_US
dc.identifier.pmid17895399-
dc.identifier.scopuseid_2-s2.0-38149004331en_US
dc.identifier.hkuros143173-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-38149004331&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume83en_US
dc.identifier.issue1en_US
dc.identifier.spage173en_US
dc.identifier.epage180en_US
dc.identifier.eissn1938-3673-
dc.identifier.isiWOS:000251834100021-
dc.publisher.placeUnited Statesen_US
dc.identifier.issnl0741-5400-

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