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The Journal of Immunology, 2005, 174: 3158-3163.
Copyright © 2005 by The American Association of Immunologists

CUTTING EDGE

Cutting Edge: Recent Immune Status Determines the Source of Antigens That Drive Homeostatic T Cell Expansion1

William C. Kieper2,*, Amy Troy{dagger}, J. Theodore Burghardt*, Chris Ramsey*, Joon Youb Lee*, Han-Qing Jiang{ddagger}, Wolfgang Dummer3,*, Hao Shen{dagger}, John J. Cebra{ddagger} and Charles D. Surh4,*

* Department of Immunology, The Scripps Research Institute, La Jolla, CA 92037; {dagger} Department of Microbiology, School of Medicine, and {ddagger} Department of Biology, University of Pennsylvania, Philadelphia, PA 19104

Homeostatic proliferation of naive T cells transferred to T cell-deficient syngeneic mice is driven by low-affinity self-MHC/peptide ligands and the cytokine IL-7. In addition to homeostatic proliferation, a subset of naive T cells undergoes massive proliferation in chronically immunodeficient hosts, but not in irradiated normal hosts. Such rapid T cell proliferation occurs largely independent of homeostatic factors, because it was apparent in the absence of IL-7 and in T cell-sufficient hosts devoid of functional T cell immunity. Strikingly, immunodeficient mice raised under germfree conditions supported only slow homeostatic proliferation, but not the marked T cell proliferation observed in conventionally raised immunodeficient mice. Thus, polyclonal naive T cell expansion in T cell-deficient hosts can be driven predominantly by either self-Ags or foreign Ags depending on the host’s previous state of T cell immunocompetency.




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