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The Journal of Immunology, 2005, 175: 6428-6435.
Copyright © 2005 by The American Association of Immunologists

CD11chigh Dendritic Cell Ablation Impairs Lymphopenia-Driven Proliferation of Naive and Memory CD8+ T Cells1

Tami Zaft2,*, Anita Sapoznikov2,*, Rita Krauthgamer*, Dan R. Littman{dagger} and Steffen Jung3,*

* Department of Immunology, The Weizmann Institute of Science, Rehovot, Israel; and {dagger} Howard Hughes Medical Institute, Skirball Institute of Biomolecular Medicine, New York University School of Medicine, New York, NY 10016

The peripheral lymphocyte pool size is governed by homeostatic mechanisms. Thus, grafted T cells expand and replenish T cell compartments in lymphopenic hosts. Lymphopenia-driven proliferation of naive CD8+ T cells depends on self-peptide/MHC class I complexes and the cytokine IL-7. Lymphopenia-driven proliferation and maintenance of memory CD8+ T cells are MHC independent, but are believed to require IL-7 and contact with a bone marrow-derived cell that presents the cytokine IL-15 by virtue of its high affinity receptor (IL-15R{alpha}). In this study we show that optimal spontaneous proliferation of grafted naive and memory CD8+ T cells in mice rendered lymphopenic through gene ablation or irradiation requires the presence of CD11chigh dendritic cells. Our results suggest a dual role of CD11chigh dendritic cells as unique APC and cytokine-presenting cells.


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