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Inflammation controls B lymphopoiesis by regulating chemokine CXCL12 expression.

dc.contributor.author Foster, SJ
dc.contributor.author Kelsoe, Garnett
dc.contributor.author Kondo, M
dc.contributor.author Ueda, Y
dc.contributor.author Yang, K
dc.coverage.spatial United States
dc.date.accessioned 2015-11-18T16:44:45Z
dc.date.issued 2004-01-05
dc.identifier https://www.ncbi.nlm.nih.gov/pubmed/14707114
dc.identifier 199/1/47
dc.identifier.issn 0022-1007
dc.identifier.uri http://hdl.handle.net/10161/10909
dc.description.abstract Inflammation removes developing and mature lymphocytes from the bone marrow (BM) and induces the appearance of developing B cells in the spleen. BM granulocyte numbers increase after lymphocyte reductions to support a reactive granulocytosis. Here, we demonstrate that inflammation, acting primarily through tumor necrosis factor alpha (TNFalpha), mobilizes BM lymphocytes. Mobilization reflects a reduced CXCL12 message and protein in BM and changes to the BM environment that prevents homing by cells from naive donors. The effects of TNFalpha are potentiated by interleukin 1 beta (IL-1beta), which acts primarily to expand the BM granulocyte compartment. Our observations indicate that inflammation induces lymphocyte mobilization by suppressing CXCL12 retention signals in BM, which, in turn, increases the ability of IL-1beta to expand the BM granulocyte compartment. Consistent with this idea, lymphocyte mobilization and a modest expansion of BM granulocyte numbers follow injections of pertussis toxin. We propose that TNFalpha and IL-1beta transiently specialize the BM to support acute granulocytic responses and consequently promote extramedullary lymphopoiesis.
dc.language eng
dc.relation.ispartof J Exp Med
dc.relation.isversionof 10.1084/jem.20031104
dc.subject Adoptive Transfer
dc.subject Animals
dc.subject Antigens, CD
dc.subject B-Lymphocytes
dc.subject Bone Marrow Cells
dc.subject Chemokine CXCL12
dc.subject Chemokines, CXC
dc.subject Colony-Forming Units Assay
dc.subject Female
dc.subject Gene Expression Regulation
dc.subject Inflammation
dc.subject Mice
dc.subject Mice, Inbred C57BL
dc.subject Mice, Knockout
dc.subject Receptors, Tumor Necrosis Factor
dc.subject Receptors, Tumor Necrosis Factor, Type I
dc.subject Receptors, Tumor Necrosis Factor, Type II
dc.subject Stromal Cells
dc.title Inflammation controls B lymphopoiesis by regulating chemokine CXCL12 expression.
dc.type Journal article
pubs.author-url https://www.ncbi.nlm.nih.gov/pubmed/14707114
pubs.begin-page 47
pubs.end-page 58
pubs.issue 1
pubs.organisational-group Basic Science Departments
pubs.organisational-group Duke
pubs.organisational-group Duke Cancer Institute
pubs.organisational-group Duke Human Vaccine Institute
pubs.organisational-group Immunology
pubs.organisational-group Institutes and Centers
pubs.organisational-group School of Medicine
pubs.publication-status Published
pubs.volume 199


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