The Journal of Experimental Medicine
VeriKine-HS Human IFN-Beta
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Published online 21 August 2000.
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© The Rockefeller University Press, 0022-1007/2000/8/557/ $5.00
The Journal of Experimental Medicine, Volume 192, Number 4, August 21, 2000 557-564

Original Article

Naive T Cells Transiently Acquire a Memory-like Phenotype during Homeostasis-Driven Proliferation

Ananda W. Goldratha, Lisa Y. Bogatzkia, and Michael J. Bevana

a Department of Immunology and Howard Hughes Medical Institute, University of Washington, Seattle, Washington 98195
Howard Hughes Medical Institute, University of Washington, Box 357370, Seattle, WA 98195.206-685-3612206-685-3610

mbevan{at}u.washington.edu

In a depleted lymphoid compartment, naive T cells begin a slow proliferation that is independent of cognate antigen yet requires recognition of major histocompatibility complex–bound self-peptides. We have followed the phenotypic and functional changes that occur when naive CD8+ T cells undergo this type of expansion in a lymphopenic environment. Naive T cells undergoing homeostasis-driven proliferation convert to a phenotypic and functional state similar to that of memory T cells, yet distinct from antigen-activated effector T cells. Naive T cells dividing in a lymphopenic host upregulate CD44, CD122 (interleukin 2 receptor β) and Ly6C expression, acquire the ability to rapidly secrete interferon {gamma}, and become cytotoxic effectors when stimulated with cognate antigen. The conversion of naive T cells to cells masquerading as memory cells in response to a homeostatic signal does not represent an irreversible differentiation. Once the cellularity of the lymphoid compartment is restored and the T cells cease their division, they regain the functional and phenotypic characteristics of naive T cells. Thus, homeostasis-driven proliferation provides a thymus-independent mechanism for restoration of the naive compartment after a loss of T cells.

Key Words: lymphopenia • transgenic • Ly6C • CD44

Abbreviations used in this paper: B6, C57BL/6; RAG, recombination activating gene.

© 2000 The Rockefeller University Press


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