Under conditions of lymphopenia, transferred naive T cells can undergo marked proliferation (1, 2) as a result of both T cell–receptor engagement and cytokine stimulation. Naive T cells that undergo this homeostatic proliferation also acquire characteristics of memory and effector cells as measured by phenotype, by hypersensitivity to antigen stimulation, and by increased production of IFN-γ. This phenomenon has been observed following the adoptive transfer of either naive, transgenic T cells or of polyclonal, wild-type T cells. Recent studies using recombination-activating gene-deficient (Rag–/–) mice, CD3εdeficient mice, and irradiated normal mice as recipients have shown that memory T cells do not revert to naive T cells under these conditions to fill the peripheral naive T cell pool, as originally postulated. Rather, after lymphopenia, homeostasis-driven proliferation restores only the memory T cell compartment, whereas thymopoiesis is required to reconstitute the naive T cell compartment (3, 4). Cytokines and dendritic cells contribute to the induction and maintenance of homeostatic T cell proliferation. Using a coculture system without foreign antigen, Ge et al.(5) demonstrated that such proliferation requires interaction of the T cell receptor with self-peptide MHCs on dendritic cells. In vitro, this response also requires dendritic cell-derived IL-15 and can be inhibited by the introduction of CD4+CD25+ regulatory T cells. In animals recovering from lymphopenia following bone marrow transplantation (BMT), dendritic cells also expedite T cell reconstitution and activation (6, 7). Recent studies show that IL-7 and IL-15 jointly regulate homeostatic proliferation of memory phenotype CD8+ T cells (8, 9), whereas IL-7 on its own enhances naive T cell survival (10).