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Article: Impaired V(D)J recombination and increased apoptosis among B cell precursors in the bone marrow of c-Abl-deficient mice

TitleImpaired V(D)J recombination and increased apoptosis among B cell precursors in the bone marrow of c-Abl-deficient mice
Authors
Issue Date2007
PublisherOxford University Press. The Journal's web site is located at http://intimm.oxfordjournals.org/
Citation
International Immunology, 2007, v. 19 n. 3, p. 267-276 How to Cite?
AbstractPrevious studies on c-Abl-deficient mice have shown high post-natal mortality and lymphopenia. However, the mechanisms by which c-Abl may influence B lymphopoiesis remain obscure. In this study, we analyzed B cell sub-populations at various differentiation stages in the bone marrow (BM) of c-Abl-deficient mice. Phenotypic analyses revealed that c-Abl-/- pro-B cells were reduced to half of normal incidence and absolute number, while pre-B cells showed an even greater reduction. Both c-Abl-/- pro-B and pre-B cell populations showed considerably elevated apoptosis ex vivo and in short-term culture but their cell cycle progression was not impaired. In contrast, apoptosis of immature IgM+IgD- B lymphocytes remained at normal control levels. Inhibition of c-Abl activity by STI571 in normal BM cultures significantly increased apoptosis in B cell precursors while the survival of immature B cells was not affected. To determine whether c-Abl deficiency affects Ig heavy-chain rearrangement, we found that the frequency of V(D)J recombination was markedly reduced by 15-fold in c-Abl-/- pro-B cells compared with the control values. However, no perturbation in the levels of signal-end recombination intermediates was found. Taken together, we propose that c-Abl mediates a stage-specific anti-apoptotic response in precursor B cells and is required for efficient V(D)J recombination during B cell development. © 2007 Oxford University Press.
Persistent Identifierhttp://hdl.handle.net/10722/78810
ISSN
2015 Impact Factor: 3.031
2015 SCImago Journal Rankings: 1.613
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLam, QLKen_HK
dc.contributor.authorLo, CKCen_HK
dc.contributor.authorZheng, BJen_HK
dc.contributor.authorKo, KHen_HK
dc.contributor.authorOsmond, DGen_HK
dc.contributor.authorWu, GEen_HK
dc.contributor.authorRottapel, Ren_HK
dc.contributor.authorLu, Len_HK
dc.date.accessioned2010-09-06T07:47:05Z-
dc.date.available2010-09-06T07:47:05Z-
dc.date.issued2007en_HK
dc.identifier.citationInternational Immunology, 2007, v. 19 n. 3, p. 267-276en_HK
dc.identifier.issn0953-8178en_HK
dc.identifier.urihttp://hdl.handle.net/10722/78810-
dc.description.abstractPrevious studies on c-Abl-deficient mice have shown high post-natal mortality and lymphopenia. However, the mechanisms by which c-Abl may influence B lymphopoiesis remain obscure. In this study, we analyzed B cell sub-populations at various differentiation stages in the bone marrow (BM) of c-Abl-deficient mice. Phenotypic analyses revealed that c-Abl-/- pro-B cells were reduced to half of normal incidence and absolute number, while pre-B cells showed an even greater reduction. Both c-Abl-/- pro-B and pre-B cell populations showed considerably elevated apoptosis ex vivo and in short-term culture but their cell cycle progression was not impaired. In contrast, apoptosis of immature IgM+IgD- B lymphocytes remained at normal control levels. Inhibition of c-Abl activity by STI571 in normal BM cultures significantly increased apoptosis in B cell precursors while the survival of immature B cells was not affected. To determine whether c-Abl deficiency affects Ig heavy-chain rearrangement, we found that the frequency of V(D)J recombination was markedly reduced by 15-fold in c-Abl-/- pro-B cells compared with the control values. However, no perturbation in the levels of signal-end recombination intermediates was found. Taken together, we propose that c-Abl mediates a stage-specific anti-apoptotic response in precursor B cells and is required for efficient V(D)J recombination during B cell development. © 2007 Oxford University Press.en_HK
dc.languageengen_HK
dc.publisherOxford University Press. The Journal's web site is located at http://intimm.oxfordjournals.org/en_HK
dc.relation.ispartofInternational Immunologyen_HK
dc.rightsInternational Immunology. Copyright © Oxford University Press.en_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshApoptosis - geneticsen_HK
dc.subject.meshB-Lymphocytes - cytology - metabolismen_HK
dc.subject.meshBone Marrow Cells - cytology - metabolismen_HK
dc.subject.meshCell Cycle - geneticsen_HK
dc.subject.meshCell Differentiation - geneticsen_HK
dc.subject.meshCell Lineage - geneticsen_HK
dc.subject.meshCells, Cultureden_HK
dc.subject.meshGene Rearrangement, B-Lymphocyteen_HK
dc.subject.meshImmunoglobulin Heavy Chains - geneticsen_HK
dc.subject.meshLymphopoiesis - geneticsen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Knockouten_HK
dc.subject.meshPhenotypeen_HK
dc.subject.meshProto-Oncogene Proteins c-abl - deficiency - geneticsen_HK
dc.subject.meshRecombination, Geneticen_HK
dc.subject.meshVDJ Recombinases - metabolismen_HK
dc.titleImpaired V(D)J recombination and increased apoptosis among B cell precursors in the bone marrow of c-Abl-deficient miceen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0953-8178&volume=19&issue=3&spage=267&epage=76&date=2007&atitle=Impaired+V(D)J+recombination+and+increased+apoptosis+among+B+cell+precursors+in+the+bone+marrow+of+c-Abl-deficient+mice.en_HK
dc.identifier.emailLam, QLK: qlam@pathology.hku.hken_HK
dc.identifier.emailZheng, BJ: bzheng@hkucc.hku.hken_HK
dc.identifier.emailLu, L: liweilu@hkucc.hku.hken_HK
dc.identifier.authorityLam, QLK=rp00312en_HK
dc.identifier.authorityZheng, BJ=rp00353en_HK
dc.identifier.authorityLu, L=rp00477en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1093/intimm/dxl143en_HK
dc.identifier.pmid17229817en_HK
dc.identifier.scopuseid_2-s2.0-33847345575en_HK
dc.identifier.hkuros126174en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33847345575&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume19en_HK
dc.identifier.issue3en_HK
dc.identifier.spage267en_HK
dc.identifier.epage276en_HK
dc.identifier.isiWOS:000244429500005-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridLam, QLK=8722491000en_HK
dc.identifier.scopusauthoridLo, CKC=24825171000en_HK
dc.identifier.scopusauthoridZheng, BJ=7201780588en_HK
dc.identifier.scopusauthoridKo, KH=7202688627en_HK
dc.identifier.scopusauthoridOsmond, DG=7101898926en_HK
dc.identifier.scopusauthoridWu, GE=7404976456en_HK
dc.identifier.scopusauthoridRottapel, R=7004089740en_HK
dc.identifier.scopusauthoridLu, L=7403963552en_HK
dc.identifier.citeulike1132711-

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