The JI PBL Intereron Source
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     
 

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Norian, L. A.
Right arrow Articles by Allen, P. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Norian, L. A.
Right arrow Articles by Allen, P. M.
The Journal of Immunology, 2004, 173: 835-844.
Copyright © 2004 by The American Association of Immunologists

No Intrinsic Deficiencies in CD8+ T Cell-Mediated Antitumor Immunity with Aging1

Lyse A. Norian and Paul M. Allen2

Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110

Aging is associated with a decline in immune function, particularly within the T cell compartment. Because CD8+ T cells are critical mediators of protective immunity against cancer, which arises more frequently with advancing age, it is important to understand how aging affects T cell-based antitumor responses. We used our DUC18 T cell/CMS5 tumor model system to examine the ability of both aged APCs and aged, tumor-specific CD8+ T cells to mount protective responses to tumors in vivo. An assessment of aged DUC18 T cells in vitro showed a naive phenotype, but impaired proliferation in response to anti-CD3 and anti-CD28 stimulation. We found that DCs from young and old recipient mice are comparable phenotypically, and endogenous APCs in these mice are equally able to prime adoptively transferred young DUC18 T cells. Even when aged DUC18 T cells are transferred into aged CMS5-challenged mice, Ag-specific proliferation and CD25 expression are similar to those found when young DUC18 T cells are transferred into young mice. Although trafficking to tumor sites appears unequal, old and young DUC18 T cells reject primary CMS5 challenges to the same degree and with similar kinetics. Overall, we found no loss of endogenous APC function or intrinsic defects in CD8+ DUC18 T cells with advanced age. Therefore, when young and old tumor-specific T cell populations are equivalently sized, CD8+ T cell-mediated antitumor immunity in our system is not impaired by age, a finding that has positive implications for T cell-based immunotherapies.




This article has been cited by other articles:


Home page
 J. Immunol.Home page
B.-C. Chiu, V. R. Stolberg, and S. W. Chensue
Mononuclear Phagocyte-Derived IL-10 Suppresses the Innate IL-12/IFN-{gamma} Axis in Lung-Challenged Aged Mice
J. Immunol., September 1, 2008; 181(5): 3156 - 3166.
[Abstract] [Full Text] [PDF]

Home page
 J. Gerontol. A Biol. Sci. Med. Sci.Home page
A. Grolleau-Julius, M. R. Garg, R. Mo, L. L. Stoolman, and R. L. Yung
Effect of Aging on Bone Marrow-Derived Murine CD11c+CD4-CD8{alpha}- Dendritic Cell Function.
J. Gerontol. A Biol. Sci. Med. Sci., October 1, 2006; 61(10): 1039 - 1047.
[Abstract] [Full Text] [PDF]

Home page
 Sci Aging Knowl EnvironHome page
Papers of Note
Sci. Aging Knowl. Environ., July 14, 2004; 2004(28): nw27 - nw27.
[Full Text]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Website Copyright © 2004 by The American Association of Immunologists, Inc. All rights reserved.
All Contents Copyright © 2004 by The American Association of Immunologists, Inc. All rights reserved.