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Published online before print May 17, 2005

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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.1104669

Received for publication November 18, 2004.
Revised April 21, 2005.
Accepted for publication April 22, 2005.

Article

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

Bennett D. Elzey ^*, Julieann F. Grant , Haley W. Sinn ^*, Bernhard Nieswandt , Thomas J. Waldschmidt , and Timothy L. Ratliff ^*¶||**@

Departments of *Urology, Pathology, Interdisciplinary Immunology Program, and **Microbiology, Carver College of Medicine, Medical Scientist Training Program, ^¶Prostate Cancer Research Group, and Holden Comprehensive Cancer Center, University of Iowa, Iowa City; Rudolf Virchow Center for Experimental Biomedicine, University of Wurzburg, Germany; and ||Iowa City Veterans Affairs Medical Center, Iowa City

^@ To whom correspondence should be addressed. E-mail: tim-ratliff{at}uiowa.edu.

	Abstract

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-derived 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 humoral immunity.

Key Words: B cells • humoral immunity • mouse • innate immunity • knockout

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