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* Centre National de la Recherche Scientifique, Unité Mixte de Recherche 8527, Institut de Biologie de Lille/Institut Pasteur de Lille,
Unité 547, Institut National de la Santé et de la Recherche Médicale, Institut Pasteur de Lille, and
Laboratoire d’Immunologie, Equipe Associée 2686, Centre Hospitalier Universitaire and Université de Lille 2, Lille, France; and
Centre National de la Recherche Scientifique, Unité Mixte de Recherche 6101, Faculté de Médecine de Limoges, Université de Limoges, Centre Hospitalier Universitaire Dupuytren, Laboratoire d’Hématologie, Limoges, France
There is a finely tuned interplay between immune and neuroendocrine systems. Metabolic disturbances like obesity will have serious consequences on immunity both at the cellular and at the cytokine expression levels. Our in vivo results confirm the immune deficiency of ob/ob mice, leptin deficient and massively obese, characterized by a reduced Ag-specific T cell proliferation after keyhole limpet hemocyanin immunization. In this report, we show that dendritic cells (DCs), major APCs involved in T lymphocyte priming, are affected in obese mice. Both their function and their steady-state number are disturbed. We demonstrate that DCs from ob/ob mice are less potent in stimulation of allogenic T cells in vitro. This impaired functionality is not associated with altered expression of phenotypic markers but with the secretion of immunosuppressive cytokines such as TGF-
. Moreover, we show increased in vivo steady-state number of epidermal DCs in ob/ob mice, which is not due to a migratory defect. The ob/ob mice are characterized by the absence of functional leptin, a key adipokine linking nutrition, metabolism, and immune functions. Interestingly, intradermal injection of leptin is able to restore epidermal DC number in obese mice. Thus, DCs might be directly sensitive to metabolic disturbances, providing a partial explanation of the immunodeficiency associated with obesity.
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 grants from the Centre National de la Recherche Scientifique, the Université Lille II, and from the Institut Pasteur de Lille. L.M. and T.-S.O. are doctoral fellows of the Ministère de l’Education Nationale, de la Recherche et de la Technologie.
2 Current address: Laboratoire de Neuroimmunoendocrinologie, Institut Pasteur de Lille, 59019 Lille cedex, France.
3 Address correspondence and reprint requests to Dr. Isabelle Wolowczuk, Laboratoire de Neuroimmunoendocrinologie/Institut Pasteur de Lille, 1, Rue Albert Calmette, Boite Postale 447, 59019 Lille cedex, France. E-mail address: isabelle.wolowczuk{at}ibl.fr
4 Abbreviations used in this paper: DC, dendritic cell; KLH, keyhole limpet hemocyanin; LC, Langerhans cell; BM-dDC, bone marrow-derived DC; CT, control; MHCII, MHC class II.
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