期刊
BLOOD
卷 111, 期 10, 页码 5028-5036出版社
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2007-06-097410
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资金
- NIAID NIH HHS [R01 AI060924] Funding Source: Medline
- NIDDK NIH HHS [DK071712, K01 DK071712, K01 DK067338, DK067338-02] Funding Source: Medline
- NIGMS NIH HHS [T32 GM007337] Funding Source: Medline
Although mounting evidence indicates that platelets participate in the modulation of both innate and adaptive immunity, the mechanisms by which platelets exert these effects have not been clearly defined. The study reported herein uses a previously documented adoptive transfer model to investigate the ability of platelet-derived membrane vesicles to communicate activation signals to the B-cell compartment. The findings demonstrate for the first time that platelet-derived membrane vesicles are sufficient to deliver CD154 to stimulate antigen-specific IgG production and modulate germinal center formation through cooperation with responses elicited by CD4(+) T cells. The data are consistent with the hypothesis that platelets modulate inflammation and adaptive immunity at sites distant from the location of activation and that platelet-derived membrane vesicles are sufficient to mediate the effect.
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