title: Maternal autoimmune thyroid disease and the fetal immune system.
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.
  
  
  METHODS
  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.
authors.affiliation: Cellular Autoimmunity Unit, Department of Clinical Sciences, Lund University, Malmö University Hospital, Sweden.
authors.forename: J
authors.initials: J
authors.lastname: Svensson
authors.forename: C
authors.initials: C
authors.lastname: Oderup
authors.forename: C
authors.initials: C
authors.lastname: Akesson
authors.forename: K
authors.initials: K
authors.lastname: Uvebrant
authors.forename: B
authors.initials: B
authors.lastname: Hallengren
authors.forename: U B
authors.initials: UB
authors.lastname: Ericsson
authors.forename: J
authors.initials: J
authors.lastname: Arvastsson
authors.forename: J S
authors.initials: JS
authors.lastname: Danska
authors.forename: M
authors.initials: M
authors.lastname: Lantz
authors.forename: C M
authors.initials: CM
authors.lastname: Cilio
mesh_terms: D001323:Autoantibodies / Q000097:blood / Q000276:immunology*; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology*; D016207:Cytokines / Q000097:blood / Q000276:immunology; D005260:Female; D005312:Fetal Blood / Q000276:immunology; D005333:Fetus / Q000276:immunology*; D006801:Humans; D007231:Infant, Newborn; D018836:Inflammation Mediators / Q000097:blood / Q000276:immunology; D007694:Killer Cells, Natural / Q000276:immunology*; D008297:Male; D008431:Maternal-Fetal Exchange / Q000276:immunology*; D011247:Pregnancy; D011248:Pregnancy Complications / Q000097:blood / Q000276:immunology*; D013967:Thyroiditis, Autoimmune / Q000097:blood / Q000276:immunology*
chemical_list: D001323:Autoantibodies; D016207:Cytokines; D018836:Inflammation Mediators