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

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

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Publication Type:: Journal Article
Citation:: Journal of Experimental Medicine, 2000, 191 (5), pp. 771 - 780
Issue Date:: 2000-03-06

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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.

Please use this identifier to cite or link to this item:

http://hdl.handle.net/10453/8687