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Modulation of the neonatal T cell-me...

The Pennsylvania State University.

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Modulation of the neonatal T cell-mediated immune response by maternally derived stress hormones.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Modulation of the neonatal T cell-mediated immune response by maternally derived stress hormones./
作者:	Zahwa, Hassan.
面頁冊數:	294 p.
附註:	Source: Dissertation Abstracts International, Volume: 69-11, Section: B, page: 6687.
Contained By:	Dissertation Abstracts International69-11B.
標題:	Biology, Microbiology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3336157
ISBN:	9780549902546

Modulation of the neonatal T cell-mediated immune response by maternally derived stress hormones.
Zahwa, Hassan.

Modulation of the neonatal T cell-mediated immune response by maternally derived stress hormones. - 294 p.

Source: Dissertation Abstracts International, Volume: 69-11, Section: B, page: 6687.

Thesis (Ph.D.)--The Pennsylvania State University, 2008.

A simple National Library of Medicine title search for the term "psychological stress" returns over 1400 titles, the majority of which address the impact of stress on the adult immune system. Despite this plethora of psychological stress-related publications, only a handful address the impact of stress on neonatal immunity. Neonates are vaccinated within days of delivery to generate an immune response that is maintained in some instances for the remainder of the individual's life. Neonates begin to receive vaccinations while they are almost entirely dependent on their mother for nutrition and care. Maternally derived hormones, reflecting the mother's psychological and physical conditions, are passed to the neonate via the breast milk. This passage could potentially expose the neonate to several immunomodulatory hormones, namely glucocorticoids and epinephrine. These hormones are known to hinder the adult immune response in the context of infection. The neonate is no exception, as exposure to maternally derived stress hormones hinders the primary T cell-mediated adaptive immune response to herpes simplex virus type-1 infection (HSV-1). Neonatal exposure to stress-like levels of glucocorticoids increased HSV-related morbidity and mortality via type II glucocorticoid receptor-dependent mechanisms. When examined ex vivo, this exposure (1) reduced overall splenic cellularity, (2) hindered the ability of CTL to expand clonally, (3) to express adequate levels of IL2Ralpha, (4) to lyse HSV-infected cells, and (5) and to produce pro-inflammatory cytokines. The hindrance of the primary immune response to HSV-1 infection is extended to the CTL memory repertoire. Moreover, these effects on the primary and memory HSV-specific T cell repertoires were reversed with the administration of a glucocorticoid receptor antagonist, which also prevented the HSV-related mortality. These findings demonstrate a role for glucocorticoids in the modulation of the neonatal immune system in response to infection. Given that current neonatal immunization practices do not account for environmental factors at the time of immunization, these findings warrant an in-depth review of the clinical practices related to neonatal immunization. Moreover, these findings also shed light on the importance of managing post-partum maternal stress as exposure of the neonate to maternally derived hormones imprints the neonate's immune system with both immediate and lifelong consequences.

ISBN: 9780549902546Subjects--Topical Terms:

1017734
Biology, Microbiology.

Modulation of the neonatal T cell-mediated immune response by maternally derived stress hormones.
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