Milk: a postnatal imprinting system stabilizing FoxP3 expression and regulatory T cell differentiation

Please use this identifier to cite or link to this item:
https://osnadocs.ub.uni-osnabrueck.de/handle/urn:nbn:de:gbv:700-2016072714699
Open Access logo originally created by the Public Library of Science (PLoS)
Full metadata record
DC FieldValueLanguage
dc.creatorMelnik, Bodo C.
dc.creatorJohn, Swen Malte
dc.creatorCarrera-Bastos, Pedro
dc.creatorSchmitz, Gerd
dc.date.accessioned2016-07-27T09:39:33Z
dc.date.available2016-07-27T09:39:33Z
dc.date.issued2016-07-27T09:39:33Z
dc.identifier.citationClinical and Translational Allergy 6:18, 2016; London : BioMedCentral
dc.identifier.urihttps://repositorium.ub.uni-osnabrueck.de/handle/urn:nbn:de:gbv:700-2016072714699-
dc.description.abstractBackground: Breastfeeding has protective effects for the development of allergies and atopy. Recent evidence underlines that consumption of unboiled farm milk in early life is a key factor preventing the development of atopic diseases. Farm milk intake has been associated with increased demethylation of FOXP3 and increased numbers of regulatory T cells (Tregs). Thus, the questions arose which components of farm milk control the differentiation and function of Tregs, critical T cell subsets that promote tolerance induction and inhibit the development of allergy and autoimmunity. Findings: Based on translational research we identified at least six major signalling pathways that could explain milk’s biological role controlling stable FoxP3 expression and Treg differentiation: (1) via maintaining appropriate magnitudes of Akt‑mTORC1 signalling, (2) via transfer of milk fat‑derived long‑chain ω‑3 fatty acids, (3) via transfer of milk‑derived exosomal microRNAs that apparently decrease FOXP3 promoter methylation, (4) via transfer of exosomal transforming growth factor‑β, which induces SMAD2/SMAD3‑dependent FoxP3 expression, (5) via milk‑derived Bifidobacterium and Lactobacillus species that induce interleukin‑10 (IL‑10)‑mediated differentiation of Tregs, and (6) via milk‑derived oligosaccharides that serve as selected nutrients for the growth of bifidobacteria in the intestine of the new born infant. Conclusion:Accumulating evidence underlines that milk is a complex signalling and epigenetic imprinting network that promotes stable FoxP3 expression and long‑lasting Treg differentiation, crucial postnatal events preventing atopic and autoimmune diseases.eng
dc.relationhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC4864898/pdf/13601_2016_Article_108.pdf
dc.rightsNamensnennung 4.0 International-
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/-
dc.subjectEpigeneticeng
dc.subjectExosomeeng
dc.subjectFoxP1eng
dc.subjectFoxP3eng
dc.subjectMilkeng
dc.subjectMicroRNAeng
dc.subjectmTORC1eng
dc.subjectProbioticseng
dc.subjectTGF-ßeng
dc.subjectTregeng
dc.subject.ddc610 - Medizin und Gesundheit
dc.titleMilk: a postnatal imprinting system stabilizing FoxP3 expression and regulatory T cell differentiationeng
dc.typeEinzelbeitrag in einer wissenschaftlichen Zeitschrift [article]
dc.identifier.doi10.1186/s13601-016-0108-9
vCard.ORGFB8
Appears in Collections:FB08 - Hochschulschriften
Open-Access-Publikationsfonds

Files in This Item:
File Description SizeFormat 
Clinical_and_Translational_Allergy_Melnik_13601_2016_Article_108.pdf1,27 MBAdobe PDF
Clinical_and_Translational_Allergy_Melnik_13601_2016_Article_108.pdf
Thumbnail
View/Open


This item is licensed under a Creative Commons License Creative Commons