The Journal of Experimental Medicine
Torrey Pines Biolabs
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents
This Article
Right arrow Full Text
Right arrow Full Text (PDF, 122K)
Right arrow Alert me when this article is cited
Right arrow Citation Map
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new content in the JEM
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Smyth, M. J.
Right arrow Articles by Godfrey, D. I.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Smyth, M. J.
Right arrow Articles by Godfrey, D. I.
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?
© The Rockefeller University Press, 0022-1007/2000/2/661/ $5.00
The Journal of Experimental Medicine, Volume 191, Number 4, February 21, 2000 661-668

Original Article

Differential Tumor Surveillance by Natural Killer (NK) and NKT Cells

Mark J. Smytha, Kevin Y. T. Thiaa, Shayna E.A. Streeta, Erika Cretneya, Joseph A. Trapania, Masaru Taniguchib, Tetsu Kawanob, Sonja B. Pelikanc, Nadine Y. Crowec, and Dale I. Godfreyc
a From the Cellular Cytotoxicity Laboratory, Austin Research Institute, Austin and Repatriation Medical Centre, Heidelberg, 3084 Victoria, Australia
b Division of Molecular Immunology, Center of Biomedical Sciences, School of Medicine, Chiba University, Chiba 260-8670, Japan
c Department of Pathology and Immunology, Monash University Medical School, Prahran, 3181 Victoria, Australia

Correspondence to: Mark J. Smyth, Cellular Cytotoxicity Laboratory, Austin Research Institute, Austin and Repatriation Medical Centre, Studley Rd., Heidelberg, 3084 Victoria, Australia. Tel:61-39-287-0653 Fax:61-39-287-0600 E-mail:m.smyth{at}ari.unimelb.edu.au.

Natural tumor surveillance capabilities of the host were investigated in six different mouse tumor models where endogenous interleukin (IL)-12 does or does not dictate the efficiency of the innate immune response. Gene-targeted and lymphocyte subset–depleted mice were used to establish the relative importance of natural killer (NK) and NK1.1+ T (NKT) cells in protection from tumor initiation and metastasis. In the models examined, CD3- NK cells were responsible for tumor rejection and protection from metastasis in models where control of major histocompatibility complex class I–deficient tumors was independent of IL-12. A protective role for NKT cells was only observed when tumor rejection required endogenous IL-12 activity. In particular, T cell receptor J{alpha}281 gene-targeted mice confirmed a critical function for NKT cells in protection from spontaneous tumors initiated by the chemical carcinogen, methylcholanthrene. This is the first description of an antitumor function for NKT cells in the absence of exogenously administered potent stimulators such as IL-12 or {alpha}-galactosylceramide.

Key Words: tumor immunity, perforin, natural killer T cells, interleukin 12, carcinogen


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?


This article has been cited by other articles:



  Home | Help | Feedback | Subscriptions | Archive | Search
TABLE OF CONTENTS