Journal article
Actin integrity is indispensable for CD95/Fas-induced apoptosis of HIV-specific CD8(+) T cells
Apoptosis (London), v 12(12), pp 2175-2186
01 Dec 2007
PMID: 17891455
Featured in Collection : UN Sustainable Development Goals @ Drexel
Abstract
We have recently provided data suggesting a potential role for mitochondria and Bcl-2-family molecules in apoptosis sensitivity of HIV-specific CD8(+) T cells. Here, we report on the role of filamentous (F) actin in this process. Disruption of actin by cytochalasin D (cytD) or lantrunculin A remarkably reduced CD95/Fas-induced apoptosis of HIV-specific CD8(+) T cells while their spontaneous apoptosis was unaffected. This inhibition cannot be attributed to changes of CD95/Fas distribution or levels in these cells. Furthermore, cytD treatment reduced CD95/Fas-induced apoptosis of CD8(+) T cells from HIV+ patients independently of their differentiation status. CD95/Fas-induced apoptosis of both CD38(+) and CD38(-) HIV-specific CD8(+) T cells was inhibited by cytD treatment indicating that actin mediates this apoptotic process independently of the activation level of these cells. CytD was found to reduce the activation of caspase-8 induced by short treatment of purified CD8(+) T cells from HIV+ patients with anti-CD95/Fas. Our data reveal actin as a critical mediator of HIV-specific CD8(+) T cell apoptosis; further analysis of the molecular mechanisms governing this process may potentially contribute to design new therapies targeting the enhancement of the immune system in HIV infection.
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Details
- Title
- Actin integrity is indispensable for CD95/Fas-induced apoptosis of HIV-specific CD8(+) T cells
- Creators
- Constantinos Petrovas - Drexel UniversityYvonne M. Mueller - Drexel UniversityGuibin Yang - Drexel UniversitySusan R. Altork - Drexel UniversityJeffrey M. Jacobson - Drexel UniversityPeter G. Pitsakis - Drexel UniversityKaram C. Mounzer - Philadelphia FightJohn D. Altman - Emory UniversityPeter D. Katsikis - Drexel University
- Publication Details
- Apoptosis (London), v 12(12), pp 2175-2186
- Publisher
- Springer Nature
- Number of pages
- 12
- Grant note
- R01AI052005 / 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 AI52005; R01 AI46719 / 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:000250784400005
- Scopus ID
- 2-s2.0-35948985062
- Other Identifier
- 991019335232904721
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- Collaboration types
- Domestic collaboration
- Web of Science research areas
- Biochemistry & Molecular Biology
- Cell Biology