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Blood, 27 August 2009, Vol. 114, No. 9, pp. 1784-1793. Prepublished online as a Blood First Edition Paper on June 26, 2009; DOI 10.1182/blood-2008-12-192120. This Article Full Text Full Text (PDF) Supplemental Figures All Versions of this Article: blood-2008-12-192120v1 114/9/1784    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Le Campion, A. Articles by Lucas, B. Search for Related Content PubMed PubMed Citation Articles by Le Campion, A. Articles by Lucas, B. Related Collections Immunobiology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Lymphopenia-induced spontaneous T-cell proliferation as a cofactor for autoimmune disease development Armelle Le Campion1,2, Marie-Claude Gagnerault3, Cédric Auffray1,2, Chantal Bécourt3, Maud Poitrasson-Rivière1,2, Eliette Lallemand1,2, Boris Bienvenu1,2, Bruno Martin1,2, Françoise Lepault1,2, and Bruno Lucas1,2 1 Institut Cochin, Université Paris Descartes, Centre National de la Recherche Scientifique Unité Mixte de Recherche 8104, Cochin Hospital, Paris; 2 Inserm Unité 567, Cochin Hospital, Paris; and 3 Inserm Unité 561, Saint-Vincent-de-Paul Hospital, Paris, France Lymphopenia is thought to be a major cause of tolerance breakdown. In a lymphopenic environment, self-recognition events induce some T cells to expand strongly (a mechanism known as spontaneous proliferation). In this study, we show that in C57BL/6 mice, the repertoire resulting from lymphopenia-induced spontaneous CD4+ T-cell proliferation included a proportion of regulatory T cells as large as that observed in a normal mouse, and no autoimmune disorder was observed. By contrast, in nonobese diabetic mice, differences in the ability of conventional and regulatory T cells to expand in response to lymphopenia led to an unbalance between these 2 T-cell compartments at the expense of regulatory T cells, resulting in the onset of autoimmune diseases. Notably, this accounted for the rapid transfer of diabetes with small numbers of BDC2.5 CD4+ T cells. Thus, lymphopenia does not itself induce autoimmunity, but it should be considered as a cofactor for the development of autoimmune disorders. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

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