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Review
Antenatal risk factors, cytokines and the development of atopic disease in early childhood
  1. E K Chung1,
  2. R L Miller2,
  3. M T Wilson3,
  4. S J McGeady4,
  5. J F Culhane5
  1. 1The Division of General Pediatrics, Department of Pediatrics, Jefferson Medical College, Philadelphia, Pennsylvania, USA; AI duPont Hospital for Children, Wilmington, Delaware, USA
  2. 2The Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, Columbia University College of Physicians and Surgeons, New York, New York, USA
  3. 3Harvard College, Cambridge, Massachusetts, USA; The Nemours Summer Research Scholar Program, AI duPont Hospital for Children, Wilmington, Delaware
  4. 4The Division of Allergy and Immunology, Department of Pediatrics, Jefferson Medical College, Philadelphia, Pennsylvania, USA; AI duPont Hospital for Children, Wilmington, Delaware
  5. 5The Department of Obstetric and Gynecology, Drexel University College of Medicine, Philadelphia, Pennsylvania, USA
  1. Correspondence to:
    E K Chung
    Jefferson Pediatrics/duPont Children’s Health Program, 833 Chestnut Street, Suite 300, Philadelphia, PA 19107, USA; echung{at}nemours.org

Abstract

Atopic diseases are complex entities influenced by an array of risk factors, including genetic predisposition, environmental allergens, antenatal exposures, infections and psychosocial factors. One proposed mechanism by which these risk factors contribute to the development of atopic disease is through changes in the production of T helper cell type 1 (Th1) and T helper cell type 2 (Th2) cytokines. The objectives of this review are to discuss antenatal exposures that are associated with paediatric atopic diseases, to discuss the influence of the intrauterine environment on neonatal immune responses, to provide an overview of the Th1 and Th2 pathways and how they relate to atopic disease, and to summarise our current understanding of the association between cytokine responses in cord blood and the development of atopic disease in early childhood.

  • CBMC, cord blood mononuclear cell
  • IFN, interferon
  • IL, interleukin
  • PBMC, peripheral blood mononuclear cell
  • Th1, T helper cell type 1
  • Th2, T helper cell type 2
  • TNF, tumour necrosis factor

https://doi.org/10.1136/adc.2006.106492

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    Footnotes

    • Competing interests: None declared.