Reversible defects in natural killer and memory CD8 T cell lineages in interleukin 15-deficient mice
Kennedy, MK
Glaccum, M
Brown, SN
Butz, EA
Viney, JL
Embers, M
Matsuki, N
Charrier, K
Sedger, L
Willis, CR
Brasel, K
Morrissey, PJ
Stocking, K
Schuh, JACL
Joyce, S
Peschon, JJ
- Publication Type:
- Journal Article
- Citation:
- Journal of Experimental Medicine, 2000, 191 (5), pp. 771 - 780
- Issue Date:
- 2000-03-06
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Full metadata record
Field | Value | Language |
---|---|---|
dc.contributor.author | Kennedy, MK | en_US |
dc.contributor.author | Glaccum, M | en_US |
dc.contributor.author | Brown, SN | en_US |
dc.contributor.author | Butz, EA | en_US |
dc.contributor.author | Viney, JL | en_US |
dc.contributor.author | Embers, M | en_US |
dc.contributor.author | Matsuki, N | en_US |
dc.contributor.author | Charrier, K | en_US |
dc.contributor.author |
Sedger, L https://orcid.org/0000-0003-1009-5683 |
en_US |
dc.contributor.author | Willis, CR | en_US |
dc.contributor.author | Brasel, K | en_US |
dc.contributor.author | Morrissey, PJ | en_US |
dc.contributor.author | Stocking, K | en_US |
dc.contributor.author | Schuh, JACL | en_US |
dc.contributor.author | Joyce, S | en_US |
dc.contributor.author | Peschon, JJ | en_US |
dc.date.issued | 2000-03-06 | en_US |
dc.identifier.citation | Journal of Experimental Medicine, 2000, 191 (5), pp. 771 - 780 | en_US |
dc.identifier.issn | 0022-1007 | en_US |
dc.identifier.uri | http://hdl.handle.net/10453/8687 | |
dc.description.abstract | C57BL/6 mice genetically deficient in interleukin 15 (IL-15(-/-) mice) were generated by gene targeting. IL-15(-/-) mice displayed marked reductions in numbers of thymic and peripheral natural killer (NK) T cells, memory phenotype CD8+ T cells, and distinct subpopulations of intestinal intraepithelial lymphocytes (IELs). The reduction but not absence of these populations in IL-15(-/-) mice likely reflects an important role for IL-15 for expansion and/or survival of these cells. IL-15(-/-) mice lacked NK cells, as assessed by both immunophenotyping and functional criteria, indicating an obligate role for IL-15 in the development and functional maturation of NK cells. Specific defects associated with IL-15 deficiency were reversed by in vivo administration of exogenous IL-15. Despite their immunological defects, IL-15(-/-) mice remained healthy when maintained under specific pathogen-free conditions. However, IL-l5(-/-) mice are likely to have compromised host defense responses to various pathogens, as they were unable to mount a protective response to challenge with vaccinia virus. These data reveal critical roles for IL-15 in the development of specific lymphoid lineages. Moreover, the ability to rescue lymphoid defects in IL-15(-/-) mice by IL-15 administration represents a powerful means by which to further elucidate the biological roles of this cytokine. | en_US |
dc.relation.ispartof | Journal of Experimental Medicine | en_US |
dc.relation.isbasedon | 10.1084/jem.191.5.771 | en_US |
dc.subject.classification | Immunology | en_US |
dc.subject.mesh | Lymph Nodes | en_US |
dc.subject.mesh | Spleen | en_US |
dc.subject.mesh | Thymus Gland | en_US |
dc.subject.mesh | Killer Cells, Natural | en_US |
dc.subject.mesh | CD8-Positive T-Lymphocytes | en_US |
dc.subject.mesh | Epithelial Cells | en_US |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Mice, Inbred C57BL | en_US |
dc.subject.mesh | Mice | en_US |
dc.subject.mesh | Mice, Mutant Strains | en_US |
dc.subject.mesh | Vaccinia | en_US |
dc.subject.mesh | Receptors, Interleukin-2 | en_US |
dc.subject.mesh | Interleukin-15 | en_US |
dc.subject.mesh | Organ Size | en_US |
dc.subject.mesh | Lymphocyte Count | en_US |
dc.subject.mesh | Immunologic Memory | en_US |
dc.subject.mesh | Cell Lineage | en_US |
dc.subject.mesh | Female | en_US |
dc.subject.mesh | Male | en_US |
dc.subject.mesh | Receptors, Interleukin-15 | en_US |
dc.title | Reversible defects in natural killer and memory CD8 T cell lineages in interleukin 15-deficient mice | en_US |
dc.type | Journal Article | |
utslib.citation.volume | 5 | en_US |
utslib.citation.volume | 191 | en_US |
utslib.for | 060103 Cell Development, Proliferation and Death | en_US |
utslib.for | 060506 Virology | en_US |
utslib.for | 11 Medical and Health Sciences | en_US |
dc.location.activity | ISI:000085810000004 | 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 | open_access | |
pubs.issue | 5 | en_US |
pubs.publication-status | Published | en_US |
pubs.volume | 191 | en_US |
Abstract:
C57BL/6 mice genetically deficient in interleukin 15 (IL-15(-/-) mice) were generated by gene targeting. IL-15(-/-) mice displayed marked reductions in numbers of thymic and peripheral natural killer (NK) T cells, memory phenotype CD8+ T cells, and distinct subpopulations of intestinal intraepithelial lymphocytes (IELs). The reduction but not absence of these populations in IL-15(-/-) mice likely reflects an important role for IL-15 for expansion and/or survival of these cells. IL-15(-/-) mice lacked NK cells, as assessed by both immunophenotyping and functional criteria, indicating an obligate role for IL-15 in the development and functional maturation of NK cells. Specific defects associated with IL-15 deficiency were reversed by in vivo administration of exogenous IL-15. Despite their immunological defects, IL-15(-/-) mice remained healthy when maintained under specific pathogen-free conditions. However, IL-l5(-/-) mice are likely to have compromised host defense responses to various pathogens, as they were unable to mount a protective response to challenge with vaccinia virus. These data reveal critical roles for IL-15 in the development of specific lymphoid lineages. Moreover, the ability to rescue lymphoid defects in IL-15(-/-) mice by IL-15 administration represents a powerful means by which to further elucidate the biological roles of this cytokine.
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