title: T cell subsets in cord blood are influenced by maternal allergy and associated with atopic dermatitis.
abstract: BACKGROUND
  This study aimed to investigate the influence of maternal allergy on cord blood regulatory and effector T cells and to evaluate their role as a predictor of atopic dermatitis (AD) during the first 2 yr of life.
  
  
  METHODS
  Seventy mother-infant pairs were recruited in this prospective birth cohort study (21 allergic and 49 non-allergic mothers). Cord blood samples were collected and assayed for the percentage of regulatory T cells (Treg), interferon-γ (IFN-γ), and interleukin-4 (IL-4) producing T cells (Th1 and Th2, respectively) using flow cytometry. Experiments were undertaken to assess the function of cord blood CD4(+) CD25(+) CD127(-) Treg cells by cell proliferation and cytokine responses. Their offspring at the age of 2 yr old were evaluated by dermatologists to determine whether they had AD.
  
  
  RESULTS
  During the first 2 yr of life, 15.7% of the children developed a physician-diagnosed AD. A significantly increased percentage of Th2 cell was observed in cord blood of newborns with maternal allergy. Treg/Th2 ratio significantly decreased among the offspring of allergic mothers. Treg cell-associated suppression of Th2 response was attenuated in Der p1-stimulated CD4(+) CD25(-) T cells from the offspring of allergic mothers. Children with reduced Th1/Th2 (p = 0.001, OR = 0.37) and Treg/Th2 (p = 0.001, OR = 0.47) ratio in cord blood had a higher risk of developing AD.
  
  
  CONCLUSIONS
  Maternal allergic status is associated with increased percentage of IL-4(+) CD4(+) T cells and a reduced Treg/Th2 ratio in cord blood at their children's birth, which may predispose to an increased risk for developing AD.
authors.affiliation: Department of Gynaecology and Obstetrics, Beijing TongRen Hospital, Capital Medical University, Beijing, China.
authors.forename: Yujing
authors.initials: Y
authors.lastname: Fu
authors.forename: Hongfei
authors.initials: H
authors.lastname: Lou
authors.forename: Chengshuo
authors.initials: C
authors.lastname: Wang
authors.forename: Wei
authors.initials: W
authors.lastname: Lou
authors.forename: Yang
authors.initials: Y
authors.lastname: Wang
authors.forename: Tao
authors.initials: T
authors.lastname: Zheng
authors.forename: Luo
authors.initials: L
authors.lastname: Zhang
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000097:blood; D049109:Cell Proliferation; D002478:Cells, Cultured; D016009:Chi-Square Distribution; D002675:Child, Preschool; D003876:Dermatitis, Atopic / Q000175:diagnosis / Q000276:immunology*; D005260:Female; D005312:Fetal Blood / Q000166:cytology / Q000276:immunology*; D005434:Flow Cytometry; D006801:Humans; D006967:Hypersensitivity / Q000175:diagnosis / Q000276:immunology*; D007231:Infant, Newborn; D007371:Interferon-gamma / Q000097:blood; D053645:Interleukin-2 Receptor alpha Subunit / Q000097:blood; D015847:Interleukin-4 / Q000097:blood; D053699:Interleukin-7 Receptor alpha Subunit / Q000097:blood; D016015:Logistic Models; D008213:Lymphocyte Activation; D009035:Mothers; D016017:Odds Ratio; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D011446:Prospective Studies; D018570:Risk Assessment; D012307:Risk Factors; D016176:T-Lymphocyte Subsets / Q000276:immunology*; D050378:T-Lymphocytes, Regulatory / Q000276:immunology; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology
chemical_list: D015415:Biomarkers; C573415:IFNG protein, human; C508017:IL2RA protein, human; C508598:IL4 protein, human; D053645:Interleukin-2 Receptor alpha Subunit; D053699:Interleukin-7 Receptor alpha Subunit; D015847:Interleukin-4; D007371:Interferon-gamma