Journal article
Late signals from CD27 prevent Fas-dependent apoptosis of primary CD8(+) T cells
The Journal of immunology (1950), v 180(5), pp 2912-2921
01 Mar 2008
PMID: 18292513
Featured in Collection : UN Sustainable Development Goals @ Drexel
Abstract
The role of costimulation has previously been confined to the very early stages of the CD8(+) T cell response. In this study, we demonstrate the requirement for CD27 costimulation during the later phase, but not programming of the primary CD8(+) T cell response to influenza virus and reveal a novel mechanism of action for CD27 costimulation. CD27 signals, during the later phase of the primary CD8(+) T cell response, prevent apoptosis of Ag-specific CD8(+) T cells. Blocking CD27L (CD70) on days 6 and 8 after infection reduces the number of NP(366-374)-specific CD8(+) T cells, increases their sensitivity to CD95/Fas-mediated apoptosis, and up-regulates FasL on CD4(+) T cells. This reduction of NP(366-374)-specific CD8(+) T cells requires the presence of CD4(+) T cells and Fas signaling. Lack of CD27 signals also decreases the quality of memory CD8(+) T cell responses. Memory CD8(+) T cells, which express surface CD27 similar to naive cells, however, do not require CD27 costimulation during a secondary response. Thus, CD27 acts indirectly to regulate primary Ag-specific CD8(+) T cell responses by preventing apoptosis of CD8(+) T cells during the later phase of the primary response and is required for optimal quality of memory cells, but is not required during normally primed secondary CD8(+) T cell responses.
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Details
- Title
- Late signals from CD27 prevent Fas-dependent apoptosis of primary CD8(+) T cells
- Creators
- Douglas V. Dolfi - Drexel UniversityAlina C. Boesteanu - Drexel UniversityConstantinos Petrovas - Drexel UniversityDong Xia - Amgen (Australia)Eric A. Butz - Amgen (United States)Peter D. Katsikis - Drexel University
- Publication Details
- The Journal of immunology (1950), v 180(5), pp 2912-2921
- Publisher
- American Association of Immunologists
- Number of pages
- 10
- Grant note
- R01AI066215 / NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Institute of Allergy & Infectious Diseases (NIAID) R01 AI046719; R01 AI066215-03; R01 AI066215; R01 AI046719-10; R01 AI66215 / NIAID NIH HHS; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Institute of Allergy & Infectious Diseases (NIAID)
- Resource Type
- Journal article
- Language
- English
- Web of Science ID
- WOS:000256730000028
- Scopus ID
- 2-s2.0-49149109920
- Other Identifier
- 991019339575804721
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- Collaboration types
- Industry collaboration
- Domestic collaboration
- Web of Science research areas
- Immunology