Document Detail


Impairment of T-regulatory cells in cord blood of atopic mothers.
MedLine Citation:
PMID:  18539197     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Maternal atopy is a strong predictor for the development of childhood allergic diseases. The underlying mechanisms are ill defined, yet regulatory T (Treg) and T(H)17 cells may play a key role potentially shaping the early immune system toward a proallergic or antiallergic immune regulation. OBJECTIVE: We examined T(H)1/T(H)2, Treg, and T(H)17 cell responses to innate (lipid A/peptidoglycan) and mitogen/adaptive (phytohemagglutinin/Dermatophagoides pteronyssinus 1) immune stimulation in cord blood from offspring of atopic/nonatopic mothers. METHODS: Cord blood mononuclear cells from 161 healthy neonates (59% nonatopic, 41% atopic mothers) were investigated regarding Treg and T(H)17 cells (mRNA/surface markers), suppressive function, and proliferation/cytokine secretion. RESULTS: Cord blood from offspring of atopic mothers showed fewer innate-induced Treg cells (CD4(+)CD25(+)high), lower mRNA expression of associated markers (glucocorticoid-induced tumor necrosis factor receptor-related protein/lymphocyte activation gene 3; P < .05), and a trend toward lower Forkhead box transcription factor 3 (Foxp3) expression. Treg cell function was impaired in mitogen-induced suppression of T effector cells in cord blood of offspring from atopic mothers (P = .03). Furthermore, IL-10 and IFN-gamma secretion were decreased in innate-stimulated cord blood of offspring from atopic mothers (P = .04/.05). Innate-induced IL-17 was independent of maternal atopy and highly correlated with IL-13 secretion. CONCLUSION: In offspring of atopic mothers, Treg cell numbers, expression, and function were impaired at birth. T(H)17 cells were correlated with T(H)2 cells, independently of maternal atopy.
Authors:
Bianca Schaub; Jing Liu; Sabine Höppler; Severine Haug; Christine Sattler; Anna Lluis; Sabina Illi; Erika von Mutius
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of allergy and clinical immunology     Volume:  121     ISSN:  1097-6825     ISO Abbreviation:  J. Allergy Clin. Immunol.     Publication Date:  2008 Jun 
Date Detail:
Created Date:  2008-06-09     Completed Date:  2008-07-01     Revised Date:  2008-12-10    
Medline Journal Info:
Nlm Unique ID:  1275002     Medline TA:  J Allergy Clin Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1491-9, 1499.e1-13     Citation Subset:  AIM; IM    
Affiliation:
Department of Pulmonary and Allergy, University Children's Hospital Munich, Munich, Germany. Bianca.Schaub@med.uni-muenchen.de
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MeSH Terms
Descriptor/Qualifier:
Adult
Antigens, CD / biosynthesis
Cytokines / biosynthesis
Female
Fetal Blood / cytology,  immunology*
Flow Cytometry
Forkhead Transcription Factors / biosynthesis
Gene Expression
Humans
Hypersensitivity, Immediate / immunology*
Infant, Newborn / immunology*
Male
Mothers
RNA, Messenger / analysis
Receptors, Nerve Growth Factor / biosynthesis
Receptors, Tumor Necrosis Factor / biosynthesis
Reverse Transcriptase Polymerase Chain Reaction
T-Lymphocyte Subsets / immunology*
T-Lymphocytes, Regulatory / immunology*
Transforming Growth Factor beta / biosynthesis
Chemical
Reg. No./Substance:
0/Antigens, CD; 0/Cytokines; 0/FOXP3 protein, human; 0/Forkhead Transcription Factors; 0/RNA, Messenger; 0/Receptors, Nerve Growth Factor; 0/Receptors, Tumor Necrosis Factor; 0/TNFRSF18 protein, human; 0/Transforming Growth Factor beta; 0/cytotoxic T-lymphocyte antigen 4
Comments/Corrections
Comment In:
J Allergy Clin Immunol. 2008 Oct;122(4):841; author reply 841   [PMID:  19014775 ]

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