File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Apoptosis and its modulation during B lymphopoiesis in mouse bone marrow

TitleApoptosis and its modulation during B lymphopoiesis in mouse bone marrow
Authors
Issue Date2000
PublisherBlackwell Munksgaard. The Journal's web site is located at http://www.blackwellpublishing.com/journals/IMR
Citation
Immunological Reviews, 2000, v. 175, p. 158-174 How to Cite?
AbstractStudies in normal, gene-deleted, transgenic and mutant mice have examined apoptotic cell death and its role in B lymphopoiesis in bone marrow. Apoptotic activity has been quantitated among phenotypically defined populations of precursor B cells using flow cytometry of apoptotic cells and an established model of B-cell development. In normal mice, the frequencies of apoptotic cells (apoptotic index) and accumulation of apoptotic cells during short-term culture (apoptotic rate) are maximal at around the pro/pre-B-cell transition and among immature B lymphocytes. The brief period between onset of apoptosis and clearance by macrophages (apoptotic transit time) is similar for most precursor B-cells. Apoptosis-modulating factors produce substantial changes in apoptotic activity among pro-B and pre-B cells, associated with altered expression of bcl-2 family proteins. Pro-B-cell apoptosis, normally extensive, is markedly suppressed in the absence of p53. Complete pro-B-cell abortion in RAG-2 deletion provides an assay for apoptotic fractions in other experimental systems. Pre-B-cell apoptosis is enhanced by deficiencies of interleukin (IL)-7, Abl protooncogene or colony-stimulating factor (CSF)-1 and overexpression of heat-stable antigen, and is inhibited by IL-7 and p190(bcr/abl) transgenes. CSF-1 and melatonin administration inhibit pre-B-cell apoptosis, probably via stromal cell stimulation. Such apoptotic modulation has implications for B-cell homeostasis, quality control, immunodeficiency and neoplasia.
Persistent Identifierhttp://hdl.handle.net/10722/88791
ISSN
2015 Impact Factor: 9.542
2015 SCImago Journal Rankings: 7.059
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLu, Len_HK
dc.contributor.authorOsmond, DGen_HK
dc.date.accessioned2010-09-06T09:48:02Z-
dc.date.available2010-09-06T09:48:02Z-
dc.date.issued2000en_HK
dc.identifier.citationImmunological Reviews, 2000, v. 175, p. 158-174en_HK
dc.identifier.issn0105-2896en_HK
dc.identifier.urihttp://hdl.handle.net/10722/88791-
dc.description.abstractStudies in normal, gene-deleted, transgenic and mutant mice have examined apoptotic cell death and its role in B lymphopoiesis in bone marrow. Apoptotic activity has been quantitated among phenotypically defined populations of precursor B cells using flow cytometry of apoptotic cells and an established model of B-cell development. In normal mice, the frequencies of apoptotic cells (apoptotic index) and accumulation of apoptotic cells during short-term culture (apoptotic rate) are maximal at around the pro/pre-B-cell transition and among immature B lymphocytes. The brief period between onset of apoptosis and clearance by macrophages (apoptotic transit time) is similar for most precursor B-cells. Apoptosis-modulating factors produce substantial changes in apoptotic activity among pro-B and pre-B cells, associated with altered expression of bcl-2 family proteins. Pro-B-cell apoptosis, normally extensive, is markedly suppressed in the absence of p53. Complete pro-B-cell abortion in RAG-2 deletion provides an assay for apoptotic fractions in other experimental systems. Pre-B-cell apoptosis is enhanced by deficiencies of interleukin (IL)-7, Abl protooncogene or colony-stimulating factor (CSF)-1 and overexpression of heat-stable antigen, and is inhibited by IL-7 and p190(bcr/abl) transgenes. CSF-1 and melatonin administration inhibit pre-B-cell apoptosis, probably via stromal cell stimulation. Such apoptotic modulation has implications for B-cell homeostasis, quality control, immunodeficiency and neoplasia.en_HK
dc.languageengen_HK
dc.publisherBlackwell Munksgaard. The Journal's web site is located at http://www.blackwellpublishing.com/journals/IMRen_HK
dc.relation.ispartofImmunological Reviewsen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshAntigens, CD - genetics - physiologyen_HK
dc.subject.meshAntigens, CD24en_HK
dc.subject.meshApoptosis - physiologyen_HK
dc.subject.meshB-Lymphocytes - immunologyen_HK
dc.subject.meshBone Marrow Cells - immunologyen_HK
dc.subject.meshCell Differentiationen_HK
dc.subject.meshCell Lineageen_HK
dc.subject.meshColony-Stimulating Factors - genetics - physiologyen_HK
dc.subject.meshDNA-Binding Proteins - geneticsen_HK
dc.subject.meshHomeostasisen_HK
dc.subject.meshInterleukin-7 - genetics - physiologyen_HK
dc.subject.meshMembrane Glycoproteinsen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Mutant Strainsen_HK
dc.subject.meshModels, Biologicalen_HK
dc.subject.meshProto-Oncogene Proteins c-abl - genetics - physiologyen_HK
dc.subject.meshReceptors, Antigen, B-Cell - metabolismen_HK
dc.subject.meshTumor Suppressor Protein p53 - genetics - physiologyen_HK
dc.titleApoptosis and its modulation during B lymphopoiesis in mouse bone marrowen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0105-2896&volume=175&spage=158&epage=174&date=2000&atitle=Apoptosis+and+its+modulation+during+B+lymphopoiesis+in+mouse+bone+marrowen_HK
dc.identifier.emailLu, L:liweilu@hkucc.hku.hken_HK
dc.identifier.authorityLu, L=rp00477en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1034/j.1600-065X.2000.017506.xen_HK
dc.identifier.pmid10933601-
dc.identifier.scopuseid_2-s2.0-0033933693en_HK
dc.identifier.hkuros56453en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0033933693&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume175en_HK
dc.identifier.spage158en_HK
dc.identifier.epage174en_HK
dc.identifier.isiWOS:000088202800016-
dc.publisher.placeDenmarken_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats