Cooperation between platelet-derived CD154 and CD4+ T cells for enhanced germinal center formation

被引:73
作者
Elzey, BD
Grant, JF
Sinn, HW
Nieswandt, B
Waldschmidt, TJ
Ratliff, TL
机构
[1] Univ Iowa, Dept Urol, Iowa City, IA 52242 USA
[2] Univ Iowa, Dept Pathol, Iowa City, IA 52242 USA
[3] Univ Iowa, Dept Interdisciplinary Immunol Program, Iowa City, IA 52242 USA
[4] Univ Iowa, Dept Microbiol, Iowa City, IA 52242 USA
[5] Univ Iowa, Carver Coll Med, Med Sci Training Program, Iowa City, IA 52242 USA
[6] Univ Iowa, Prostate Canc Res Grp, 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
[9] Iowa City Vet Affairs Med Ctr, Iowa City, IA USA
关键词
B cells; humoral immunity; mouse; innate immunity; knockout;
D O I
10.1189/jlb.1104669
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
It has been demonstrated previously that platelet-derived CD154 communicates with the adaptive immune compartment, enhancing B and T cell responses in CD154(-/-) mice. The presence of platelets was also shown to be necessary for optimal production of immunoglobulin G (IgG) in normal C57BL/6 mice. These data led us to hypothesize that platelets perform a sentinel function, quickly relaying activating signals to the adaptive immune compartment. Here, we report that platelet-deirived CD154 increases serum IgG levels and germinal center formation under conditions where antigen-specific CD4(+) T cell numbers are limiting. We propose that in the physiologic setting where antigen-specific B and T cells are rare, platelets function to enhance signals required for robust adaptive Immoral immunity.
引用
收藏
页码:80 / 84
页数:5
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