The Journal of Experimental Medicine
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Published 17 June 2002. doi:10.1084/jem.20020033
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© Rockefeller University Press, 0022-1007/2002/6/1515/ $5.00
The Journal of Experimental Medicine, Volume 195, Number 12, June 17, 2002 1515-1522

Cytokine Requirements for Acute and Basal Homeostatic Proliferation of Naive and Memory CD8+ T Cells

Ananda W. Goldrath1, Pallavur V. Sivakumar2, Moira Glaccum2, Mary K. Kennedy2, Michael J. Bevan3, Christophe Benoist1, Diane Mathis1 and Eric A. Butz2

1 Section on Immunology and Immunogenetics, Joslin Diabetes Center, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02215
2 Immunex Corporation, Seattle, WA 98101
3 Department of Immunology and Howard Hughes Medical Institute, University of Washington, Seattle, WA 98195

Address correspondence to Ananda Goldrath, Section of Immunology and Immunogenetics, Joslin Diabetes Center, 1 Joslin Place, Boston, MA 02215. Phone: 617-264-2786; Fax: 617-264-2744; E-mail: Ananda.Goldrath{at}joslin.harvard.edu

Both naive and memory T cells undergo antigen-independent proliferation after transfer into a T cell–depleted environment (acute homeostatic proliferation), whereas only memory T cells slowly divide in a full T cell compartment (basal proliferation). We show, first, that naive and memory CD8+ T cells have different cytokine requirements for acute homeostatic proliferation. Interleukin (IL)-7 receptor(R){alpha}–mediated signals were obligatory for proliferation of naive T cells in lymphopenic hosts, whereas IL-15 did not influence their division. Memory T cells, on the other hand, could use either IL-7R{alpha}– or IL-15–mediated signals for acute homeostatic proliferation: their proliferation was delayed when either IL-7R{alpha} was blocked or IL-15 removed, but only when both signals were absent was proliferation ablated. Second, the cytokine requirements for basal and acute homeostatic proliferation of CD8+ memory T cells differ, as basal division of memory T cells was blocked completely in IL-15–deficient hosts. These data suggest a possible mechanism for the dearth of memory CD8+ T cells in IL-15– and IL-15R{alpha}–deficient mice is their impaired basal proliferation. Our results show that naive and memory T lymphocytes differ in their cytokine dependence for acute homeostatic proliferation and that memory T lymphocytes have distinct requirements for proliferation in full versus empty compartments.

Key Words: homeostasis • IL-7 • IL-15 • T cell numbers • memory


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