TY - JOUR
T1 - Platelet-mediated modulation of adaptive immunity
T2 - A communication link between innate and adaptive immune compartments
AU - Elzey, Bennett D.
AU - Tian, Jun
AU - Jensen, Robert J.
AU - Swanson, Axel K.
AU - Lees, Jason R.
AU - Lentz, Steven R.
AU - Stein, Colleen S.
AU - Nieswandt, Bernhard
AU - Wang, Yiqiang
AU - Davidson, Beverly L.
AU - Ratliff, Timothy L.
N1 - Funding Information:
We thank Justin Fishbaugh for assistance in developing the flow cytometry parameters for detecting platelet activation. We thank Drs. Gail Bishop, Eric Brown, Thomas Ferguson, Thomas Griffith, John Harty, Thomas Waldschmidt, and Lyse Norian for helpful discussions and editorial comments on the manuscript. Also, we thank Linda Buckner for secretarial support. This work was supported by NIH grants HL63017 (S.R.L.), HL63943 (S.R.L.), DK54014 (T.L.R.), and CA096691 (T.L.R.).
PY - 2003/7/1
Y1 - 2003/7/1
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=0038445960&partnerID=8YFLogxK
U2 - 10.1016/S1074-7613(03)00177-8
DO - 10.1016/S1074-7613(03)00177-8
M3 - Article
C2 - 12871635
AN - SCOPUS:0038445960
SN - 1074-7613
VL - 19
SP - 9
EP - 19
JO - Immunity
JF - Immunity
IS - 1
ER -
