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Normal Establishment of Virus-Specific Memory CD8 T Cell Pool following Primary Infection during Pregnancy¹

Carolyn M. Constantin^*, David Masopust^2,, Tania Gourley, Jason Grayson, Ora L. Strickland^*, Rafi Ahmed and Elizabeth A. Bonney^3,

^* Nell Hodgson Woodruff School of Nursing, and Emory Vaccine Center and Department of Microbiology and Immunology, Emory University, School of Medicine, Atlanta, GA 30322; Wake Forrest School of Medicine, Winston-Salem, NC 27157; and Department of Obstetrics/Gynecology, University of Vermont College of Medicine, Burlington, VT 05401

Suppression of cell-mediated immunity has been proposed as a mechanism that promotes maternal tolerance of the fetus but also contributes to increased occurrence and severity of certain infections during pregnancy. Despite decades of research examining the effect of pregnancy on Ag-specific T cell responses, many questions remain. In particular, quantitative examination of memory CD8 T cell generation following infection during pregnancy remains largely unknown. To examine this issue, we evaluated the generation of protective immunity following infection during pregnancy with a nonpersistent strain of lymphocytic choriomeningitis virus (LCMV) in mice. The CD8 T cell response to LCMV occurred normally in pregnant mice compared with the nonpregnant cohort with rapid viral clearance in all tissues tested except for the placenta. Despite significant infiltration of CD8 T cells to the maternal-fetal interface, virus persisted in the placenta until delivery. Live pups were not infected and generated normal primary immune responses when challenged as adults. Memory CD8 T cell development in mice that were pregnant during primary infection was normal with regards to the proliferative capacity, number of Ag-specific cells, cytokine production upon re-stimulation, and the ability to protect from re-infection. These data suggest that virus-specific adaptive memory is normally generated in mice during pregnancy.

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 National Institute of Nursing Research, National Institutes of Health Training Grant F31-NR07924-02 (to C.M.C.), the American Nurses Foundation (to C.M.C.), Sigma Theta Tau, International (to C.M.C.), the National Institutes of Health Grants 1R01HD0472244 (to E.A.B.) and AI-30048 (to R.A.), and the Cancer Research Institute Postdoctoral Fellowship (to D.M.).

² Current address: Department of Microbiology, University of Minnesota, Minneapolis, MN 53455

³ Address correspondence and reprint requests to Dr. Elizabeth Bonney, Department of Obstetrics/Gynecology, University of Vermont College of Medicine, Smith 410, Medical Center Hospital of Vermont Campus, 111 Colchester Avenue, Burlington, VT 05401. E-mail address: ebonney{at}uvm.edu

⁴ Abbreviations used in this paper: CMI, cell-mediated immunity; NMS, normal mouse serum.