Fetal and neonatal IL-13 production during pregnancy and at birth and subsequent development of atopic symptoms

Citation
Tj. Williams et al., Fetal and neonatal IL-13 production during pregnancy and at birth and subsequent development of atopic symptoms, J ALLERG CL, 105(5), 2000, pp. 951-959
Citations number
32
Categorie Soggetti
Clinical Immunolgy & Infectious Disease",Immunology
Journal title
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
ISSN journal
00916749 → ACNP
Volume
105
Issue
5
Year of publication
2000
Pages
951 - 959
Database
ISI
SICI code
0091-6749(200005)105:5<951:FANIPD>2.0.ZU;2-7
Abstract
Background: Cytokine production at the materno-fetal interface may influenc e the development of atopy-predisposing immune responses. Because IL-13 pos sesses IL-4-like activity and may regulate the immune responses observed in atopy, it may contribute to the expression of the atopic phenotype initiat ed during intrauterine life. Objective: We sought to examine IL-13 expression by fetal and neonatal cell s and the placenta. Methods: The production of IL-13 by neonatal and fetal T cells was examined by culturing the cells in the presence or absence of PHA. Production of IL -13 at term was considered in the context of the later development of atopi c disease in the child, IL-13 expression in the placenta was assessed by us ing immunohistochemistry. Results: IL-13 immunoreactivity within the placenta was restricted to 16 to 27 weeks' gestation (6/6 positive vs 0/10 at >27 weeks' gestation). In con trast, spontaneous release of IL-13 by fetal mononuclear cells was first ob served from 27 weeks' gestation but was undetectable after 37 weeks' gestat ion, PHA-stimulated mononuclear cells showed increased IL-13 levels in 80% of samples. Term babies (>37 weeks' gestation) with a parental history of a topy with atopic symptoms by 3 years of age produced significantly lower co ncentrations of PHA-induced IL-13 when compared with babies with no parenta l history of atopy (P = .034). Conclusion: Thus babies at risk of atopic disease in infancy display defect ive IL-13 production at birth. This may represent an inherent immaturity in the development of T cell-cytokine responses in babies at genetic risk for atopy or could be a consequence of downregulation of responses by other fa ctors. Normal pregnancy, irrespective of atopic status, is associated with the production of appreciable quantities of IL-13 initially by the placenta and subsequently by the fetus. The regulation of this production and its c onsequences for the mother and fetus remains to be elaborated.