Abstract |
Platelets are highly reactive components of the circulatory system with well-documented hemostatic function. Recent studies extend platelet function to modulation of local inflammatory events through the release of chemokines, cytokines, and a number of immunomodulatory ligands, including CD154. We hypothesized that platelet-derived CD154 modulates adaptive immunity. The data reported herein demonstrate that platelets, via CD154, induce dendritic cell maturation, B cell isotype switching, and augment CD8(+) T cell responses both in vitro and in vivo. Platelet transfusion studies demonstrate that platelet-derived CD154 alone is sufficient to induce isotype switching and augment T lymphocyte function during viral infection, leading to enhanced protection against viral rechallenge. Additionally, depletion of platelets in normal mice results in decreased antigen-specific antibody production.
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Authors | Bennett D Elzey, Jun Tian, Robert J Jensen, Axel K Swanson, Jason R Lees, Steven R Lentz, Colleen S Stein, Bernhard Nieswandt, Yiqiang Wang, Beverly L Davidson, Timothy L Ratliff |
Journal | Immunity
(Immunity)
Vol. 19
Issue 1
Pg. 9-19
(Jul 2003)
ISSN: 1074-7613 [Print] United States |
PMID | 12871635
(Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.)
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Chemical References |
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Topics |
- Adaptation, Physiological
- Adenoviridae
(immunology)
- Animals
- Blood Platelets
(physiology)
- CD40 Ligand
(blood, physiology)
- CD8-Positive T-Lymphocytes
(immunology)
- Immunity, Innate
- Mice
- Mice, Inbred C57BL
- Virus Diseases
(immunology)
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