| First Author | Kennedy MK | Year | 2000 |
| Journal | J Exp Med | Volume | 191 |
| Issue | 5 | Pages | 771-80 |
| PubMed ID | 10704459 | Mgi Jnum | J:60915 |
| Mgi Id | MGI:1354083 | Doi | 10.1084/jem.191.5.771 |
| Citation | Kennedy MK, et al. (2000) Reversible defects in natural killer and memory CD8 T cell lineages in interleukin 15-deficient mice [see comments]. J Exp Med 191(5):771-80 |
| abstractText | 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-15(-/-) 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. |
