Control of homeostatic proliferation by regulatory T cells.

Shen S, Ding Y, Tadokoro CE, Olivares-Villagómez D, Camps-Ramírez M, Curotto de Lafaille MA, Lafaille JJ
J Clin Invest. 2005 115 (12): 3517-26

PMID: 16294223 · PMCID: PMC1283941 · DOI:10.1172/JCI25463

Homeostatic proliferation of T cells leads to the generation of effector/memory cells, which have the potential to cause harm to the host. The role of Tregs in the control of homeostatic proliferation is unclear. In this study we utilized mice that either harbor or lack Tregs as recipients of monoclonal or polyclonal T cells. We observed that while Tregs completely prevented cell division of T cells displaying low affinity for self ligands, they had a less marked, albeit significant, effect on cell cycle entry of T cells displaying higher affinity. The presence of Tregs resulted in a lower accumulation of T cells, enhanced apoptosis, and impaired differentiation to a cytokine-producing state. We conclude that Tregs play a major role in the control of homeostatic proliferation.

MeSH Terms (27)

Animals Antibodies Antibodies, Monoclonal Apoptosis CD4-Positive T-Lymphocytes CD5 Antigens Cell Proliferation Cell Separation Flow Cytometry Genes, RAG-1 Heterozygote Hyaluronan Receptors Immunologic Memory In Situ Nick-End Labeling Ligands Lymph Nodes Lymphocyte Activation Mice Mice, Inbred C57BL Mice, Transgenic Myelin Basic Protein Receptors, Antigen, T-Cell Spleen T-Lymphocytes T-Lymphocytes, Regulatory Time Factors Transgenes

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