Platelet-mediated modulation of adaptive immunity: A communication link between innate and adaptive immune compartments

被引:315
作者
Elzey, BD
Tian, J
Jensen, RJ
Swanson, KA
Lees, JR
Lentz, SR
Stein, CS
Nieswandt, B
Wang, YQ
Davidson, BL
Ratliff, TL [1 ]
机构
[1] Univ Iowa, Dept Urol, Iowa City, IA 52242 USA
[2] Univ Iowa, Prostate Canc Res Grp, Iowa City, IA 52242 USA
[3] Univ Iowa, Program Immunol, Iowa City, IA 52242 USA
[4] Iowa City Vet Affairs Med Ctr, Iowa City, IA USA
[5] Univ Iowa, Dept Internal Med, Iowa City, IA 52242 USA
[6] Univ Iowa, Dept Microbiol, Iowa City, IA 52242 USA
[7] Univ Iowa, Holden Comprehens Canc Ctr, Iowa City, IA 52242 USA
[8] Univ Wurzburg, Rudolf Virchow Ctr Expt Biomed, Wurzburg, Germany
关键词
D O I
10.1016/S1074-7613(03)00177-8
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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.
引用
收藏
页码:9 / 19
页数:11
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