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Differential tumor necrosis factor receptor 2-mediated editing of virus-specific CD8+ effector T cells

Turner, Stephen J., La Gruta, Nicole L., Stambas, John, Diaz, Gabriela and Doherty, Peter C. 2004, Differential tumor necrosis factor receptor 2-mediated editing of virus-specific CD8+ effector T cells, Proceedings of the National Academy of Sciences of the United States of America, vol. 101, no. 10, pp. 3545-3550.

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Title Differential tumor necrosis factor receptor 2-mediated editing of virus-specific CD8+ effector T cells
Author(s) Turner, Stephen J.
La Gruta, Nicole L.
Stambas, John
Diaz, Gabriela
Doherty, Peter C.
Journal name Proceedings of the National Academy of Sciences of the United States of America
Volume number 101
Issue number 10
Start page 3545
End page 3550
Publisher National Academy of Sciences
Place of publication Washington, D.C.
Publication date 2004-03-09
ISSN 0027-8424
Summary Much of the CD8+ T cell response in H2b mice with influenza pneumonia is directed at the nucleoprotein366-374 (NP366) and acid polymerase224-233 (PA224) peptides presented by the H2Db MHC class I glycoprotein. These DbNP366- and DbPA224-specific T cell populations are readily analyzed by staining with tetrameric complexes of MHC+ peptide (tetramers) or by cytokine production subsequent to in vitro stimulation with the cognate peptides. The DbPA224-specific CD8+ effector T cells make more tumor necrosis factor (TNF) α than the comparable CD8+DbNP366+ set, a difference reflected in the greater sensitivity of the CD8+DbPA224+ population to TNF receptor (TNFR) 2-mediated apoptosis under conditions of in vitro culture. Freshly isolated CD8+DbNP366+ and CD8+DbPA224+ T cells from influenza-infected TNFR2-/- mice produce higher levels of IFN-γ and TNF-α after in vitro stimulation with peptide, although the avidity of the T cell receptor-epitope interaction does not change. Increased numbers of both CD8+DbPA224+ and CD8+DbNP366+ T cells were recovered from the lungs (but not the spleens) of secondarily challenged TNFR2-/- mice, a pattern that correlates with the profiles of TNFR expression in the TNFR2+/+ controls. Thus, it seems that TNFR2-mediated editing of influenza-specific CD8+ T cells functions to limit the numbers of effectors that have localized to the site of pathology in the lung but does not modify the size of the less activated responder T cell populations in the spleen. Therefore, the massive difference in magnitude for the secondary, although not the primary, response to these DbNP366 and DbPA224 epitopes cannot be considered to reflect differential TNFR2-mediated T cell editing.
Language eng
Field of Research 110702 Applied Immunology (incl Antibody Engineering, Xenotransplantation and T-cell Therapies)
Socio Economic Objective 970111 Expanding Knowledge in the Medical and Health Sciences
HERDC Research category C1.1 Refereed article in a scholarly journal
Copyright notice ©Copyright 2004, The National Academy of Sciences
Persistent URL http://hdl.handle.net/10536/DRO/DU:30028914

Document type: Journal Article
Collection: School of Medicine
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