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The Journal of Immunology, 2007, 179, 8146-8152
Copyright © 2007 by The American Association of Immunologists, Inc.

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Pregnancy Suppresses Experimental Autoimmune Encephalomyelitis through Immunoregulatory Cytokine Production1

Melanie A. McClain, NaTosha N. Gatson, Nicole D. Powell, Tracey L. Papenfuss, Ingrid E. Gienapp, Fei Song, Todd M. Shawler, Aaron Kithcart and Caroline C. Whitacre2

Department of Molecular Virology, Immunology and Medical Genetics, The Ohio State University, Columbus, OH 43210

Women with multiple sclerosis (MS) often experience a decrease in relapse rate during pregnancy, most notably during the third trimester, with a flare of disease activity 3–6 mo postpartum. Studies in experimental autoimmune encephalomyelitis (EAE), an animal model for MS, have shown that pregnancy delays the onset and decreases the incidence of disease. We investigated the effect of pregnancy and the postpartum period in a remitting-relapsing model of murine EAE. When immunization occurs during pregnancy, mice show a reduction in the incidence of EAE as well as a decrease in clinical severity, while mice immunized during the postpartum period exhibit more severe disease. No differences in lymphocyte proliferation or expression of activation markers were noted when immunization occurred during pregnancy as compared with the nonpregnant controls. Mice immunized during pregnancy produced less TNF-{alpha} and IL-17, and showed an increased number of IL-10-secreting cells within the CD11b+, CD11c+, CD19+, and CD4+/CD25+ populations. No differences were noted in the production of IFN-{gamma}, IL-2, IL-4, and IL-5. These results suggest that when an Ag is introduced during pregnancy, an immunoregulatory rather than an immunosuppressive or Th2 environment predominates.

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 These studies were supported by grants from the National Institutes of Health (AI43376 and T32 AI 55411).

2 Address correspondence and reprint requests to Dr. Caroline C. Whitacre, Department of Molecular Virology, Immunology and Medical Genetics, College of Medicine, The Ohio State University, 260 Meiling Hall, 370 W. 9th Avenue, Columbus, OH 43210-1239. E-mail address: whitacre.3{at}osu.edu

3 Abbreviations used in this paper: MS, multiple sclerosis; EAE, experimental autoimmune encephalomyelitis; PLP, proteolipid protein; pc, post conception; MOG, myelin oligodendrocyte glycoprotein.







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