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Division of Molecular Immunology, The National Institute for Medical Research, London, United Kingdom
Lymphopenia has been associated with autoimmune pathology and it has been suggested that lymphopenia-induced proliferation of naive T cells may be responsible for the development of immune pathology. In this study we demonstrate that lymphopenia-induced proliferation is restricted to conditions of extreme lymphopenia, because neither naive nor memory T cells transferred into T cell-depleted hosts proliferate unless the depletion exceeds 90% of the peripheral repertoire. Memory CD4 T cells as well as regulatory CD4 T cells proved to be relatively resistant to depletion regimes, and both subsets restrict the expansion and phenotypic conversion of naive T cells by an IL-7R-dependent mechanism. It therefore seems unlikely that lymphopenia-induced proliferation of peripheral T cells causes deleterious side effects that result in immune pathology in states of partial and transient lymphopenia.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 This work was supported by the Medical Research Council U.K.
2 Address correspondence and reprint requests to Dr. Brigitta Stockinger, Division of Molecular Immunology, The National Institute for Medical Research, The Ridgeway, Mill Hill, London NW7 1AA, U.K. E-mail address: bstocki{at}nimr.mrc.ac.uk
3 Abbreviations used in this paper: LIP, lymphopenia-induced proliferation; Foxp3, Forkhead box P3; poly(I:C), polyinosinic acid:cytidylic acid; Tg, transgenic.
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