Transplacental priming of the human immune system with environmental allergens can occur early in gestation

Szépfalusi, Zsolt; Pichler, Josefa; Elsässer, Stefan; Duren, Katalin van; Ebner, Christof; Bernaschek, Georg; Urbanek, R.

doi:10.1067/mai.2000.108710

Cited by 102 publications

(77 citation statements)

References 32 publications

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“…The ability to demonstrate proliferative responses to allergen at birth (22,(24)(25)(26) suggests the potential occurrence of prior intrauterine exposure to allergen leading to the generation of immunological memory. Whether the responses detected by in vitro stimulation of CBMC reflect in vivo primary T cell responses merits further investigation (17,22,(26)(27)(28). Besides a genetic atopic predisposition, several allergens may also be transferred through the placenta.…”

Section: Discussionmentioning

confidence: 99%

Fetal Cord Blood: Aspects of Heightened Immune Responses

Schaub¹,

Tantisira

Gibbons

et al. 2005

J Clin Immunol

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Neonatal immune responses have been associated with the development of atopy in childhood. We assessed in cord blood mononuclear cells (CBMC) whether increased allergen/mitogen-induced lymphoproliferation (LP) is associated with pro-allergic Th2 cytokine IL-13 or Th1 cytokine IFN-γ secretion. We determined whether LP to one allergen is related to heightened lymphocyte function to other allergens/mitogen. CBMC from 135 neonates were stimulated with house dust mite (Derf1), cockroach, ovalbumin, or mitogen. LP to one allergen was associated with significantly increased LP to other allergens/mitogen. Increased Derf1-LP was associated with increased Derf1-induced IL-13 secretion (r = 0.21, p = 0.01). After adjusting for neonatal gender, race, and maternal smoking, Derf1-LP remained associated with Derf1-IL-13 (OR 3.08, 95% CI 1.56-6.10). Increased mitogeninduced proliferation was associated with increased mitogen-induced IL-13 secretion (r = 0.37, p < 0.001). For some individuals, a predisposition to a heightened immune response is already evident at birth. Whether this phenotype results in atopy in childhood warrants further investigation.

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Section: Discussionmentioning

confidence: 99%

Fetal Cord Blood: Aspects of Heightened Immune Responses

Schaub¹,

Tantisira

Gibbons

et al. 2005

J Clin Immunol

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“…Recognition and response of neonatal T lymphocytes to antigens have been previously demonstrated. [4][5][6] Fetal antigen exposure may be affected by maternal allergy status 7 and maternal exposure to high concentrations of allergen. Mothers with high cat allergen exposure also have high levels of IgG to cat and pass this specific antibody to the fetus.…”

Section: Introductionmentioning

confidence: 99%

“…15,16 While previous investigations have determined that antigen-specific T-cell priming can occur, the influence of maternal asthma and allergy on the presence and degree of CBMC proliferative response to antigens, including house dust mite, cockroach (Bla g 2), birch pollen, grass, β-lactoglobulin, and ovalbumin, has varied. [4][5][6][17][18][19] In a study of 223 neonates from Scotland, the magnitude of CBMC proliferative responses to timothy grass pollen and/or house dust mite increased in association with family history of atopic disease and/or maternal smoking. 20 We investigated the association of maternal and perinatal exposures such as maternal smoking, maternal history of asthma, eczema, hay fever, maternal weight gain during pregnancy, neonatal race/ethnicity, and Apgar scores with CBMC proliferative responses to the antigens Bla g 2, Der f 1, ovalbumin, and mitogen phytohemagglutinin.…”

Section: Introductionmentioning

confidence: 99%

Prenatal, perinatal, and heritable influences on cord blood immune responses

Willwerth

Schaub

Tantisira

et al. 2006

Annals of Allergy, Asthma & Immunology

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“…The 1998 COT recommendations embraced evidence from studies of cord blood mononuclear cell responses after stimulation with food allergens and aeroallergens. Studies since 1998 have not related maternal peanut exposure to cord blood mononuclear cell responses after stimulation with peanut allergen but suggest that the cord blood mononuclear cell responses observed after in vitro stimulation with non-peanut food allergens are not necessarily the consequence of fetal exposure to (20) , or sensitisation by (21) , maternally consumed food allergens. More direct evidence of in utero sensitisation of the fetal immune system to peanut allergen, in the form of the detection of peanut-specific IgE in cord blood, remains absent.…”

Section: Discussionmentioning

confidence: 99%

“…However, it remains unclear whether this fetal exposure results in in utero sensitisation of the fetal immune system. Moreover, it is not possible to conclude that in vitro cord blood mononuclear cell responses observed following stimulation with food proteins necessarily reflect in utero exposure (20) , in utero sensitisation (21) , or an increased risk of clinical allergy during later life (22,23) .…”

Section: Narrative Review On Cord Blood Mononuclear Cell Response To mentioning

confidence: 99%

Peanut sensitisation and allergy: influence of early life exposure to peanuts

et al. 2010

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The aim of the present systematic review was to evaluate the influence of early life exposure (maternal and childhood) to peanuts and the subsequent development of sensitisation or allergy to peanuts during childhood. Studies were identified using electronic databases and bibliography searches. Studies that assessed the impact of non-avoidance compared with avoidance or reduced quantities of peanuts or peanut products on either sensitisation or allergy to peanuts, or both outcomes, were eligible. Six human studies were identified: two randomised controlled trials, two casecontrol studies and two cross-sectional studies. In addition, published animal and mechanistic studies, relevant to the question of whether early life exposure to peanuts affects the subsequent development of peanut sensitisation, were reviewed narratively. Overall, the evidence reviewed was heterogeneous, and was limited in quality, for example, through lack of adjustment for potentially confounding factors. The nature of the evidence has therefore hindered the development of definitive conclusions. The systematic review of human studies and narrative expert-led reviews of animal studies do not provide clear evidence to suggest that either maternal exposure, or early or delayed introduction of peanuts in the diets of children, has an impact upon subsequent development of sensitisation or allergy to peanuts. Results from some animal studies (and limited evidence from human subjects) suggest that the dose of peanuts is an important mediator of peanut sensitisation and tolerance; low doses tend to lead to sensitisation and higher doses tend to lead to tolerance.Peanut allergy: Diet: Prenatal exposure: Childhood exposure Onset of peanut allergy typically occurs in childhood, with 70-100 % (1) of peanut-allergic children being reported to react upon their first known dietary exposure to peanuts. Because IgE-mediated allergic reactions require prior exposure and immunological sensitisation to the allergen, this suggests that sensitisation has already been acquired, either in utero, or by unrecognised oral exposure or non-oral (cutaneous or respiratory) routes. As many as one in fiftyfive children in the UK may currently show evidence of an allergic reaction to peanuts (2) ; indeed, peanut allergy is the most common cause of severe allergic reaction to foods, causing 30 % of all cases of anaphylaxis outside hospital (3) . Data from the Isle of Wight UK Birth Cohort Study suggest a threefold rise in the prevalence of peanut sensitisation and allergy in children born between 1989-90 and 1994 -6 (4,5) . Recent data from children born in 2001 -2 show no further increases in the prevalence of peanut sensitisation and allergy (6) .In 1998 the UK Government issued precautionary advice to mothers whose children have a family history of allergic diseases, that they may wish to avoid peanut consumption during pregnancy and breast-feeding and avoid giving the child peanuts and peanut products until the child is 3 years of age (7) . The precautionary advice was...

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Transplacental priming of the human immune system with environmental allergens can occur early in gestation

Cited by 102 publications

References 32 publications

Fetal Cord Blood: Aspects of Heightened Immune Responses

Fetal Cord Blood: Aspects of Heightened Immune Responses

Prenatal, perinatal, and heritable influences on cord blood immune responses

Peanut sensitisation and allergy: influence of early life exposure to peanuts

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