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dc.contributor.author Vasarhelyi, Barna
dc.contributor.author Tulassay, Tivadar
dc.date.accessioned 2018-02-21T11:06:16Z
dc.date.available 2018-02-21T11:06:16Z
dc.date.issued 2017
dc.identifier.citation pagination=261-266; journalVolume=229; journalIssueNumber=5; journalTitle=KLINISCHE PADIATRIE;
dc.identifier.uri http://repo.lib.semmelweis.hu//handle/123456789/4582
dc.identifier.uri doi:10.1055/s-0043-114666
dc.description.abstract In utero the skewness of the adaptive immune system towards Th2 ('antiinflammatory') direction and low of Th1/Th2 cell ratio defend the fetus against rejection by the maternal immune system. Th2 dominance at birth is also of importance as it prevents uncontrolled inflammatory processes during parturition. This condition should change rapidly after birth. In an extrauterine milieu that is inherent with exposure to microorganisms, Th1 ('proinflammatory') polarization (i. e. increased Th1 cytokine production along with high Th1/Th2 ratio) are required to maintain an efficient immune response. After birth, maternal hormone supplies including estrogen, progesterone, testosterone, and antiinflammatory prostaglandins cease abruptly. As these hormones have an immune modulatory action favoring Th2, and inhibiting Th1 polarization, their low level supports the strengthening of Th1-type immunity. During parturition a dramatic but transient increase of several hormones (oxytocin, thyorid hormones, and catecholamines) occurs. Again, the net effect of high hormone levels favors Th2 activation, followed by Th1 polarization when hormonal levels reach their postnatal levels. The perinatal change of these components results in the quick cessation of Th1 inhibition and supports the maturation of adaptive immunity to provide an effective response against extrauterine microorganisms.
dc.relation.ispartof urn:issn:0300-8630
dc.title Endocrine Factors Determining Immune Polarization during Perinatal Transition [Endokrine Faktoren und Immunpolarisierung während der perinatalen Adaptationsperiode]
dc.type Journal Article
dc.date.updated 2017-11-24T09:57:39Z
dc.language.rfc3066 en
dc.identifier.mtmt 3274342
dc.identifier.pubmed 28746946
dc.contributor.department SE/AOK/K/I. Sz. Gyermekgyógyászati Klinika
dc.contributor.department SE/AOK/I/Laboratóriumi Medicina Intézet
dc.contributor.institution Semmelweis Egyetem


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