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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.
IMMUNOBIOLOGY Expansion of CD4+CD25+ regulatory T cells by intravenous immunoglobulin: a critical factor in controlling experimental autoimmune encephalomyelitis1 Centre de Recherche des Cordeliers, Université Pierre et Marie Curie–Paris 6, Unité Mixte de Recherche (UMR) S 872, Paris, France; 2 Université Paris Descartes, UMR S 872, Paris, France; 3 Inserm U872, Paris, France; 4 Laboratory of Applied Immunology, Faculty of Public Health, Lebanese University, Beirut, Lebanon; 5 Inserm U752, University of Paris-5, Hôpital Sainte-Anne, Paris, France; 6 Unité Propre de la Recherche et de l'Enseignement Supérieur Equipe d'Accueil (UPRES-EA) 4058, Paris-Descartes University, Faculty of Medicine, Department of Internal Medicine, Cochin Hospital, Assistance Publique Hôpitaux de Paris, Paris, France; 7 Université Pierre et Marie Curie–Paris6, UMR 7087, Paris, France; and 8 Centre National de la Recherche Scientifique (CNRS), UMR 7087, Paris, France
The clinical use of intravenous immunoglobulin (IVIg) based on its immunomodulatory and anti-inflammatory potential remains an ongoing challenge. Fc
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| Copyright © 2008 by American Society of Hematology Online ISSN: 1528-0020 | |||||||||
receptor-mediated effects of IVIg, although well elucidated in certain pathologies, cannot entirely account for its proven benefit in several 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 cell (Treg) numbers and function. The protection was Treg-mediated because 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. 
