title: Maternal vitamin D intake during pregnancy increases gene expression of ILT3 and ILT4 in cord blood.
abstract: BACKGROUND
  Recent studies indicate that prenatal vitamin D intake may protect against the development of atopic diseases in young children. Vitamin D has been shown to induce tolerogenic antigen-presenting cells such as dendritic cells. Whether the allergy-protective potential of prenatal vitamin D is mediated through such mechanisms is, however, unknown.
  
  
  OBJECTIVE
  To evaluate the association between prenatal vitamin D supplementation and tolerogenic antigen-presenting cells in cord blood (CB) as determined by mRNA measurement of immunoglobulin-like transcripts (ILT)3 and ILT4.
  
  
  METHODS
  A prospective multi-centre birth cohort was established in rural areas of five European countries. Information on maternal exposures including vitamin D intake was collected by questionnaires during pregnancy. The gene expression of ILT3 and ILT4 was analysed by real-time PCR in the CB of 927 children. Maternal vitamin D supplementation was assessed in Finland and France (n=349).
  
  
  RESULTS
  Maternal vitamin D supplementation during pregnancy was associated with an increase in the gene expression of ILT3 (P=0.012) and ILT4 (P<0.001). This association remained significant for ILT4 (P=0.020) and showed a positive trend for the gene expression of ILT3 (P=0.059) after multivariate analysis controlling for various confounders.
  
  
  CONCLUSIONS
  Vitamin D supplementation during pregnancy may increase the mRNA levels of ILT3 and ILT4 in CB. This finding may point towards an early induction of tolerogenic immune responses by maternal vitamin D intake.
authors.affiliation: Children's Hospital, University of Munich, Lindwurmstrasse 4, Munich, Germany. mascha.rochat@med.uni-muenchen.de
authors.forename: M K
authors.initials: MK
authors.lastname: Rochat
authors.forename: M J
authors.initials: MJ
authors.lastname: Ege
authors.forename: D
authors.initials: D
authors.lastname: Plabst
authors.forename: J
authors.initials: J
authors.lastname: Steinle
authors.forename: S
authors.initials: S
authors.lastname: Bitter
authors.forename: C
authors.initials: C
authors.lastname: Braun-Fahrländer
authors.forename: J-C
authors.initials: JC
authors.lastname: Dalphin
authors.forename: J
authors.initials: J
authors.lastname: Riedler
authors.forename: M
authors.initials: M
authors.lastname: Roponen
authors.forename: M-R
authors.initials: MR
authors.lastname: Hirvonen
authors.forename: G
authors.initials: G
authors.lastname: Büchele
authors.forename: H
authors.initials: H
authors.lastname: Renz
authors.forename: R
authors.initials: R
authors.lastname: Lauener
authors.forename: S
authors.initials: S
authors.lastname: Krauss-Etschmann
authors.forename: E
authors.initials: E
authors.lastname: von Mutius
mesh_terms: D000328:Adult; D000938:Antigen-Presenting Cells / Q000276:immunology*; D002648:Child; D019587:Dietary Supplements; D005060:Europe / Q000453:epidemiology; D005260:Female; D005312:Fetal Blood / Q000276:immunology*; D015870:Gene Expression; D006801:Humans; D006969:Hypersensitivity, Immediate / Q000453:epidemiology / Q000276:immunology / Q000517:prevention & control*; D008297:Male; D008562:Membrane Glycoproteins / Q000235:genetics*; D011247:Pregnancy; D011446:Prospective Studies; D012333:RNA, Messenger / Q000235:genetics; D011956:Receptors, Cell Surface / Q000235:genetics*; D011971:Receptors, Immunologic / Q000235:genetics*; D012307:Risk Factors; D012424:Rural Population; D014807:Vitamin D / Q000008:administration & dosage*
chemical_list: C491341:LILRB2 protein, human; C107907:LILRB4 protein, human; D008562:Membrane Glycoproteins; D012333:RNA, Messenger; D011956:Receptors, Cell Surface; D011971:Receptors, Immunologic; D014807:Vitamin D