Innate immune surveillance of spontaneous B cell lymphomas by natural killer cells and gamma delta T cells

Street, SEA, Hayakawa, Y, Zhan, YF, Lew, AM, MacGregor, D, Jamieson, AM, Diefenbach, A, Yagita, H, Godfrey, DI and Smyth, MJ (2004) Innate immune surveillance of spontaneous B cell lymphomas by natural killer cells and gamma delta T cells. Journal of Experimental Medicine, 199 6: 879-884. doi:10.1084/jem.20031981

Attached Files (Some files may be inaccessible until you login with your UQ eSpace credentials)
Name Description MIMEType Size Downloads
UQ41141_OA.pdf Full text (open access) application/pdf 102.94KB 0

Author Street, SEA
Hayakawa, Y
Zhan, YF
Lew, AM
MacGregor, D
Jamieson, AM
Diefenbach, A
Yagita, H
Godfrey, DI
Smyth, MJ
Title Innate immune surveillance of spontaneous B cell lymphomas by natural killer cells and gamma delta T cells
Journal name Journal of Experimental Medicine   Check publisher's open access policy
ISSN 0022-1007
Publication date 2004
Sub-type Article (original research)
DOI 10.1084/jem.20031981
Open Access Status File (Publisher version)
Volume 199
Issue 6
Start page 879
End page 884
Total pages 6
Place of publication New York
Publisher Rockefeller Univ Press
Language eng
Abstract Few studies have demonstrated that innate lymphocytes play a major role in preventing spontaneous tumor formation. We evaluated the development of spontaneous tumors in mice lacking beta-2 microglobulin (beta2m; and thus MHC class I, CD1d, and CD16) and/or perform, since these tumor cells would be expected to activate innate effector cells. Approximately half the cohort of perform gene-targeted mice succumbed to spontaneous disseminated B cell lymphomas and in mice that also lacked beta2m, the lymphomas developed earlier (by more than 100 d) and with greater incidence (84%). B cell lymphomas from perforin/beta2m gene-targeted mice effectively primed cell-mediated cytotoxicity and perform, but not IFN-gamma, IL-12, or IL-18, was absolutely essential for tumor rejection. Activated NK1.1(+) and gammadeltaTCR(+) T cells were abundant at the tumor site, and transplanted tumors were strongly rejected by either, or both, of these cell types. Blockade of a number of different known costimulatory pathways failed to prevent tumor rejection. These results reflect a critical role for NK cells and gammadeltaTCP(+) T cells in innate immune surveillance of B cell lymphomas, mediated by as yet undetermined pathway(s) of tumor recognition.
Keyword Immunology
Medicine, Research & Experimental
Nk Cell
Pore-forming Protein
Deficient Mice
Tumor Surveillance
Nkt Cells
Q-Index Code C1

Document type: Journal Article
Sub-type: Article (original research)
Collections: Excellence in Research Australia (ERA) - Collection
UQ Diamantina Institute Publications
Version Filter Type
Citation counts: TR Web of Science Citation Count  Cited 122 times in Thomson Reuters Web of Science Article | Citations
Scopus Citation Count Cited 142 times in Scopus Article | Citations
Google Scholar Search Google Scholar
Created: Mon, 13 Aug 2007, 14:12:19 EST