Inflammation controls B lymphopoiesis by regulating chemokine CXCL12 expression.

dc.contributor.author

Ueda, Yoshihiro

dc.contributor.author

Yang, Kaiyong

dc.contributor.author

Foster, Sandra J

dc.contributor.author

Kondo, Motonari

dc.contributor.author

Kelsoe, Garnett

dc.coverage.spatial

United States

dc.date.accessioned

2015-11-18T16:44:45Z

dc.date.issued

2004-01-05

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.identifier

https://www.ncbi.nlm.nih.gov/pubmed/14707114

dc.identifier

199/1/47

dc.identifier.issn

0022-1007

dc.identifier.uri

https://hdl.handle.net/10161/10909

dc.language

eng

dc.publisher

Rockefeller University Press

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

Files

Original bundle

Now showing 1 - 1 of 1
Loading...
Thumbnail Image
Name:
Inflammation controls B lymphopoiesis by regulating chemokine CXCL12 expression.pdf
Size:
407.35 KB
Format:
Adobe Portable Document Format