Bone marrow B cell apoptosis during in vivo influenza virus infection requires TNF-α and lymphotoxin-α
- Publication Type:
- Journal Article
- Citation:
- Journal of Immunology, 2002, 169 (11), pp. 6193 - 6201
- Issue Date:
- 2002-12-01
Closed Access
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Full metadata record
Field | Value | Language |
---|---|---|
dc.contributor.author |
Sedger, LM |
en_US |
dc.contributor.author | Hou, S | en_US |
dc.contributor.author | Osvath, SR | en_US |
dc.contributor.author | Glaccum, MB | en_US |
dc.contributor.author | Peschon, JJ | en_US |
dc.contributor.author | Van Rooijen, N | en_US |
dc.contributor.author | Hyland, L | en_US |
dc.date.issued | 2002-12-01 | en_US |
dc.identifier.citation | Journal of Immunology, 2002, 169 (11), pp. 6193 - 6201 | en_US |
dc.identifier.issn | 0022-1767 | en_US |
dc.identifier.uri | http://hdl.handle.net/10453/18511 | |
dc.description.abstract | Suppression of bone marrow myeloid and erythroid progenitor cells occurs after infection with a variety of different viruses. In this study, we characterize the alterations in bone marrow (BM) lymphocytes after influenza virus infection in mice. We found a severe loss of BM B cells, particularly CD43Blow/-B220+ pre-B and immature B cells, in influenza virus-infected mice. Depletion of BM B lineage cells resulted primarily from cell cycle arrest and most likely apoptosis within the BM environment, rather than from increased trafficking of BM emigrants to peripheral lymphoid tissues. Use of gene-knockout mice indicates that depletion of BM B cells is dependent on TNF-α lymphotoxin-α, and both TNF receptors, TNFR1-p55 and TNFR2-p75. Thus, TNF-α and lymphotoxin-α are required for loss of BM B lineage cells during respiratory infection with influenza virus. | en_US |
dc.relation.ispartof | Journal of Immunology | en_US |
dc.subject.classification | Immunology | en_US |
dc.subject.mesh | B-Lymphocytes | en_US |
dc.subject.mesh | Killer Cells, Natural | en_US |
dc.subject.mesh | T-Lymphocyte Subsets | en_US |
dc.subject.mesh | Bone Marrow Cells | en_US |
dc.subject.mesh | Macrophages, Alveolar | en_US |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Mice, Inbred BALB C | en_US |
dc.subject.mesh | Mice, Inbred C57BL | en_US |
dc.subject.mesh | Mice, Knockout | en_US |
dc.subject.mesh | Mice | en_US |
dc.subject.mesh | Orthomyxoviridae | en_US |
dc.subject.mesh | Orthomyxoviridae Infections | en_US |
dc.subject.mesh | Tumor Necrosis Factor-alpha | en_US |
dc.subject.mesh | Receptors, Tumor Necrosis Factor | en_US |
dc.subject.mesh | Receptors, Tumor Necrosis Factor, Type I | en_US |
dc.subject.mesh | Receptors, Tumor Necrosis Factor, Type II | en_US |
dc.subject.mesh | RNA, Messenger | en_US |
dc.subject.mesh | Antigens, CD | en_US |
dc.subject.mesh | Virus Replication | en_US |
dc.subject.mesh | Cell Cycle | en_US |
dc.subject.mesh | Apoptosis | en_US |
dc.subject.mesh | Cell Differentiation | en_US |
dc.subject.mesh | Base Sequence | en_US |
dc.subject.mesh | Kinetics | en_US |
dc.subject.mesh | Lymphotoxin-alpha | en_US |
dc.title | Bone marrow B cell apoptosis during in vivo influenza virus infection requires TNF-α and lymphotoxin-α | en_US |
dc.type | Journal Article | |
utslib.citation.volume | 11 | en_US |
utslib.citation.volume | 169 | en_US |
utslib.for | 1107 Immunology | en_US |
pubs.embargo.period | Not known | en_US |
pubs.organisational-group | /University of Technology Sydney | |
pubs.organisational-group | /University of Technology Sydney/Faculty of Science | |
pubs.organisational-group | /University of Technology Sydney/Faculty of Science/School of Life Sciences | |
utslib.copyright.status | closed_access | |
pubs.issue | 11 | en_US |
pubs.publication-status | Published | en_US |
pubs.volume | 169 | en_US |
Abstract:
Suppression of bone marrow myeloid and erythroid progenitor cells occurs after infection with a variety of different viruses. In this study, we characterize the alterations in bone marrow (BM) lymphocytes after influenza virus infection in mice. We found a severe loss of BM B cells, particularly CD43Blow/-B220+ pre-B and immature B cells, in influenza virus-infected mice. Depletion of BM B lineage cells resulted primarily from cell cycle arrest and most likely apoptosis within the BM environment, rather than from increased trafficking of BM emigrants to peripheral lymphoid tissues. Use of gene-knockout mice indicates that depletion of BM B cells is dependent on TNF-α lymphotoxin-α, and both TNF receptors, TNFR1-p55 and TNFR2-p75. Thus, TNF-α and lymphotoxin-α are required for loss of BM B lineage cells during respiratory infection with influenza virus.
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