Literature DB >> 16343646

Occurrence of IgE in foals: evidence for transfer of maternal IgE by the colostrum and late onset of endogenous IgE production in the horse.

Bettina Wagner1, Julia B F Flaminio, Julie Hillegas, Wolfgang Leibold, Hollis N Erb, Douglas F Antczak.   

Abstract

IgE is the key antibody involved in type I allergies. Allergen mediated crosslinking of IgE bound to high affinity Fcepsilon-receptors on mast cells and basophils stimulates cellular degranulation and release of inflammatory mediators and cytokines. In this report, we demonstrate that IgE antibodies can be transferred from the mother to offspring in horses via the colostrum. We found a clear correlation between the IgE concentration in colostrum and the total IgE concentration in foal sera on day 2 after birth (r(sp)=0.83). Maternal IgE was detected in foal sera by ELISA and on peripheral blood leukocytes of foals by flow cytometry. Both serum and cell membrane-bound IgE were undetectable in newborn foals before colostrum uptake and peaked on days 2-5 after birth. Cell-bound IgE became undetectable at 2 months after birth. Serum IgE disappeared from the circulation within the first 3-4 months of age. These kinetics suggest that the IgE antibodies which are detectable in foals during the first 4 months after birth are of maternal origin only. The endogenous IgE production was found to begin at 9-11 months of age, when IgE could be detected on peripheral blood leukocytes and in foal sera again. After 18 months of life, the total IgE concentrations in foal sera were comparable to those detected in their dams. The late onset of endogenous IgE production offers an explanation for observations that IgE mediated allergies are generally not observed in horses before puberty. The roles of the passively transferred maternal IgE in newborn foals are not yet known, but could be manifold, ranging from passive immunity and induction of immunoregulatory functions to determinative influences of maternal IgE on the antibody repertoire in the offspring.

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Year:  2005        PMID: 16343646     DOI: 10.1016/j.vetimm.2005.10.007

Source DB:  PubMed          Journal:  Vet Immunol Immunopathol        ISSN: 0165-2427            Impact factor:   2.046


  6 in total

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  6 in total

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