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The Journal of Immunology, 2005, 174: 710-717.
Copyright © 2005 by The American Association of Immunologists

Induction of CD70 on Dendritic Cells through CD40 or TLR Stimulation Contributes to the Development of CD8+ T Cell Responses in the Absence of CD4+ T Cells1

Timothy N. J. Bullock2,* and Hideo Yagita{dagger}

* Department of Pathology and Human Immune Therapy Center, University of Virginia, Charlottesville, VA 22908; and {dagger} Department of Immunology, Juntendo University School of Medicine, Tokyo, Japan

The expansion of CD8+ T cells in response to Ag can be characterized as either dependent or independent of CD4+ T cells. The factors that influence this dichotomy are poorly understood but may be dependent upon the degree of inflammation associated with the Ag. Using dendritic cells derived from MHC class II-deficient mice to avoid interaction with CD4+ T cells in vivo, we have compared the immunogenicity of peptide-pulsed dendritic cells stimulated with molecules associated with infection to those stimulated via CD40. In the absence of CD4+ T cell help, the expansion of primary CD8+ T cells after immunization with TNF-{alpha}- or poly(I:C)-stimulated dendritic cells was minimal. In comparison, LPS- or CpG-stimulated dendritic cells elicited substantial primary CD8+ T cell responses, though not to the same magnitude generated by immunization with CD40L-stimulated dendritic cells. Remarkably, mice immunized with any stimulated dendritic cell population generated fully functional recall CD8+ T cells without the aid of CD4+ T cell help. The observed hierarchy of immunogenicity was closely correlated with the expression of CD70 (CD27L) on the stimulated dendritic cells, and Ab-mediated blockade of CD70 substantially prevented the CD4+ T cell-independent expansion of primary CD8+ T cells. These results indicate that the expression of CD70 on dendritic cells is an important determinant for helper-dependence of primary CD8+ T cell expansion and provide an explanation for the ability of a variety of pathogens to stimulate primary CD8+ T cell responses in the absence of CD4+ T cells.




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