Journal of Allergy and Clinical Immunology
Prenatal origins of allergic disease☆,☆☆,★
Section snippets
ALTERED IMMUNE RESPONSES AT BIRTH
There is a distinct need to further elucidate the factors that lead to the early development of immune responses associated with an increased risk of the development of allergic disease. It is often difficult to separate the effect of environmental conditions occurring during pregnancy from those in existence during the first months of life because they are rarely significantly different. An obvious example is cigarette smoking. Most mothers who smoke during pregnancy will continue to do so
FURTHER INVESTIGATIONS
We are currently investigating the presence of mRNA coding for IFN-γ, IL-4, IL-5, IL-10, IL-12, and IL-13 and their protein products in the fetal-placental-maternal human system in the second and third trimesters of pregnancy to determine how, and when, maternal and placental cellular responses affect the development and control of infant responses to allergens. We have preliminary evidence of CD68+ monocytes in both the maternal and fetal circulations within the placenta, indicating active
CONCLUSIONS AND HYPOTHESES
The intrauterine environment in which a fetus develops is highly biased toward TH2-like immune responses. The systems of babies with an inherited tendency toward a deficient production of IFN-γ are less likely to be able to counteract the effect of this imbalance on their own developing immune responses, particularly if the mother is also allergic and is exposed to the allergens that trigger her own allergic disease during the pregnancy. This may cause a further increase in the concentrations
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Cited by (54)
The fetal/placental weight ratio is associated with the incidence of atopic dermatitis in female infants during the first 14 months: The Hamamatsu Birth Cohort for Mothers and Children (HBC Study)
2020, International Journal of Women's DermatologyCitation Excerpt :The intrauterine environment has been increasingly implicated in the development of allergic diseases, including AD. Warner et al. (2000) showed that fetal exposure to allergens and maternoplacental–fetal immunological interactions actively contributed to whether an allergic predisposition manifests as disease after birth. Fetal growth restrictions as well as rapid catch-up growth after birth were found to predispose offspring to allergic diseases (Tedner et al., 2012).
Intrauterine sensitization of ovalbumin in the third trimester increases the risk of food allergy in progeny
2017, Saudi Journal of Biological SciencesCitation Excerpt :The immunologic mechanisms of food allergy are difficult to be identified. It has been suggested by numerous studies that the fetal period is a crucial time which determines the occurrence of allergic diseases after birth, which led to the hypothesis that the progeny has been sensitized in uterus during pregnancy (Warner et al., 2000). However, the exact crucial time of intrauterine sensitization remained to be determined (Hsu et al., 2012).
New allergies after cord blood transplantation
2013, CytotherapyCitation Excerpt :In pregnancy, the fetal-derived allogeneic tissue and maternal decidual tissue come in close contact, and yet rarely does rejection of the fetus occur. This phenomenon is attributed to the switch in T-helper-cell population of the fetoplacental unit to produce Th2 cytokines (IL-4, IL-5 and IL-10) that inhibits maternal Th1 cytokine production (IL-2, interferon [IFN]-γ) and tumor necrosis factor-β (25,26). Therefore, regardless of the mother's allergy status, the fetus is exposed to conditions that favor the development of Th2-like responses.
Developmental programming for allergy: A secondary analysis of the Mothers, Omega-3, and Mental Health Study
2013, American Journal of Obstetrics and GynecologyInduction of interleukin-4 production in neonatal IgE<sup>+</sup> cells after crosslinking of maternal IgE
2010, Developmental and Comparative Immunology
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Supported by The National Asthma Campaign, The British Lung Foundation, The David and Frederick Barclay Foundation, The British Allergy Foundation, The European Society for Pediatric Allergy and Immunology, Sandoz Pharmaceuticals, Pharmacia, and National Power.
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Reprint requests: Jill Warner, PhD, University Child Health, Level G Centre Block, Southampton General Hospital, Tremona Road, Southampton SO16 6YD United Kingdom.
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0091-6749/2000 $12.00 + 0 1/0/100088