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Blood, 15 January 2008, Vol. 111, No. 2, pp. 715-722.
Prepublished online as a Blood First Edition Paper on October 11, 2007; DOI 10.1182/blood-2007-03-079947.
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Submitted March 14, 2007
Accepted September 23, 2007
Expansion of CD4+CD25+ regulatory T cells by intravenous immunoglobulin: a critical factor in controlling experimental autoimmune encephalomyelitis
Amal Ephrem, Souleima Chamat, Catherine Miquel, Sylvain Fisson, Luc Mouthon, Giuseppina Caligiuri, Sandrine Delignat, Sriramulu Elluru, Jagadeesh Bayry, Sebastien Lacroix-Desmazes, Jose L Cohen, Benoit L Salomon, Michel D Kazatchkine, Srini V Kaveri, and Namita Misra*
Centre de Recherche des Cordeliers, Universite Pierre et Marie Curie-Paris 6, UMR S 872, Paris, France
Laboratory of Applied Immunology, Faculty of Public Health, Labanese University, Beirut, Lebanon
INSERM, U752, University of Paris-5, Hopital Sainte-Anne, Paris, France
Universite Paris Descartes, UMR S 872, Paris, France
UPRES-EA 4058, Paris-Descartes University, Faculty of Medicine, Dept of Medicine, Cochin Hospital, Assistance Publique Hopitaux de Paris, Paris, France
INSERM U872, Paris, France
CNRS, UMR 7087, Paris, France
Universite Pierre et Marie Curie-Paris 6, UMR 7087, Paris, France
* Corresponding author; email: namita.misra{at}u-psud.fr.
The clinical use of intravenous immunoglobulins (IVIg) based on its immunomodulatory and anti-inflammatory potential remains an ongoing challenge. Fc receptor-mediated effects of IVIg, though well elucidated in certain pathologies, cannot entirely account for its proven benefit in a number of autoimmune disorders mediated by autoreactive T cells. In this study, we show that prophylactic infusion of IVIg prevents the development of experimental autoimmune encephalomyelitis (EAE), an accepted animal model for multiple sclerosis (MS). The protection was associated with peripheral increase in CD4+CD25+Foxp3+ regulatory T cells (Tregs) numbers and function. The protection was Treg mediated as IVIg failed to protect against EAE in mice that were depleted of the Treg population. Rather than inducing 'de novo' generation from conventional T cells, IVIg had a direct effect on proliferation of natural Treg. In conclusion, our results highlight a novel mechanism of action of IVIg, and provide a rationale to test the use of IVIg as an immunomodulatory tool to enhance Treg in early onset MS and other autoimmune and inflammatory conditions.
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