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Effects of maternal allergen‐specific IgG in cord blood on early postnatal development of allergen‐specific T‐cell immunity
Author(s) -
Prescott S. L.,
Holt P. G.,
Jenmalm M.,
Björkstén B.
Publication year - 2000
Publication title -
allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.363
H-Index - 173
eISSN - 1398-9995
pISSN - 0105-4538
DOI - 10.1034/j.1398-9995.2000.00286.x
Subject(s) - immunology , allergen , medicine , allergy , cord blood , atopy , immunoglobulin e , immune system , antibody
Background: A wide body of epidemiologic evidence indicates that as yet unknown maternal factor(s) can influence susceptibility to allergic disease in the offspring. It is also well established that the induction of allergen‐specific T‐cell memory is frequently initiated in utero , and it is likely that maternal factors exert their influence during this period. Methods: This study examines the relationship between maternally derived allergen‐specific IgG subclass antibodies and cellular immune responses (lymphoproliferation and cytokine production) against the same allergens in 49 subjects tested at birth and at 2 years of age. Polyclonal production of the Th1 cytokine IFN‐γ was also examined in the cord‐blood samples. Results: At birth, there were positive correlations between both house‐dust mite (HDM)‐ and ovalbumin (OVA)‐specific IgG subclass levels in cord blood, maternal atopy, and the magnitude of perinatal lymphoproliferative responses to respective allergens. Inverse relationships were also observed between cord‐blood IgG antibody titres and allergen‐specific production of some Th2 cytokines. However, there were no consistent relationships between cord‐blood allergen‐specific IgG antibodies and subsequent immune responses to allergens when the same subjects were retested at 2 years of age. An inverse relationship was observed between maternal history of atopy and perinatal IFN‐γ production capacity. Conclusions: Our results suggest that transplacental transfer of allergen‐specific IgG antibody is unlikely to be a major mechanism for maternal regulation of allergen‐specific immunity in infancy. An alternative possibility is that maternal effects may operate by influencing IFN‐γ production by T cells in the offspring.