Exp Clin Endocrinol Diabetes 2011; 119(7): 445-450
DOI: 10.1055/s-0031-1279741
Article

© J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart · New York

Maternal Autoimmune Thyroid Disease and the Fetal Immune System

J. Svensson1 , 2 [*] , C. Oderup1 [*] , C. Åkesson1 , K. Uvebrant1 , B. Hallengren3 , U. B. Ericsson3 , J. Arvastsson1 , J. S. Danska4 , 5 , M. Lantz3 , C.M. Cilio1 , 2
  • 1Cellular Autoimmunity Unit, Department of Clinical Sciences, Lund University, Malmö University Hospital, Malmö, Sweden
  • 2Department of Pediatrics, Lund University, Malmö University Hospital, Malmö, Sweden
  • 3Department of Endocrinology, Lund University, Malmö University Hospital, Malmö, Sweden
  • 4Program in Developmental Biology, Hospital for Sick Children Research Institute, Toronto, ON, Canada
  • 5Department of Immunology, Faculty of Medicine, University of Toronto, Toronto, ON, Canada
Further Information

Publication History

received 29.12.2010 first decision 13.04.2011

accepted 12.05.2011

Publication Date:
10 June 2011 (online)

Abstract

Objective: Several studies indicate that in utero exposure to maternal autoimmune diseases and transplacental passage of autoantibodies affect the risk of autoimmunity in the offspring, e. g., maternally derived GAD65 autoantibody correlates with decreased risk of type 1 diabetes, whereas thyroid peroxidase autoantibody (TPOAb) positivity at birth is associated with increased incidence of autoimmune thyroid disease later in life. The aim of this study was to identify immunological changes in children born to mothers with thyroid autoimmunity that may be related to in utero exposure to autoantibodies.

Design and method: Open label prospective analysis of cord blood lymphocytes and serum cytokines by Flow Cytometry in children born to mothers with autoimmune thyroiditis (AIT) (n=31) and to healthy mothers (n=76) and titers of thyroid autoantibodies were determined in cord blood and in maternal peripheral blood at delivery.

Results: We found an increase (almost 30%) in the frequency of cord blood natural killer (NK) cells (p=0.0016) and a minor increase in the subset of T cells expressing NK markers (p=0.028), in children born to AIT mothers. There were no detectable differences in the phenotype or frequency of cord blood memory/activated T cells, including CD4+CD25+ T cells, between the 2 groups. The levels of pro-inflammatory cytokines TNF-α, IL-10, IL-12p70, IFN-γ and IL-1β were significantly decreased in offspring of AIT mothers as compared to healthy controls.

Conclusions: Maternal thyroid autoimmunity and transplacental passage of autoantibodies against thyroid antigens may affect the generation or expansion of cells with NK activity and the secretion of inflammatory cytokines.

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1 These authors contributed equally to this work.

Correspondence

M. LantzMD, PhD 

Department of Endocrinology

Malmö University Hospital

20502 Malmö

Sweden

Phone: + 46/708/202 315

Fax: + 46/337/004

Email: Mikael.Lantz@med.lu.se

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