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Gamma delta cells make a non-redunda...

Ramsburg, Elizabeth Anne.

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Gamma delta cells make a non-redundant contribution to immune responses in early life.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Gamma delta cells make a non-redundant contribution to immune responses in early life./
作者:	Ramsburg, Elizabeth Anne.
面頁冊數:	191 p.
附註:	Adviser: Adrian C. Hayday.
Contained By:	Dissertation Abstracts International63-03B.
標題:	Health Sciences, Immunology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3046214
ISBN:	049360426X

Gamma delta cells make a non-redundant contribution to immune responses in early life.
Ramsburg, Elizabeth Anne.

Gamma delta cells make a non-redundant contribution to immune responses in early life. - 191 p.

Adviser: Adrian C. Hayday.

Thesis (Ph.D.)--Yale University, 2002.

These results define a “timeline” for development of T cell responsiveness to <italic>E. vermiformis</italic> in early life and illustrate qualitative differences between immune responses in young and adult mice.

ISBN: 049360426XSubjects--Topical Terms:

1017716
Health Sciences, Immunology.

Gamma delta cells make a non-redundant contribution to immune responses in early life.
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245 1 0 $a Gamma delta cells make a non-redundant contribution to immune responses in early life.
300 $a 191 p.
500 $a Adviser: Adrian C. Hayday.
500 $a Source: Dissertation Abstracts International, Volume: 63-03, Section: B, page: 1251.
502 $a Thesis (Ph.D.)--Yale University, 2002.
520 $a These results define a “timeline” for development of T cell responsiveness to <italic>E. vermiformis</italic> in early life and illustrate qualitative differences between immune responses in young and adult mice.
520 $a γδ cells make a non-redundant contribution to the primary immune response against <italic>E. vermiformis</italic> in young mice. Among mice older than 21 days and younger than 40 days of age γδ cells are able to significantly limit parasite replication and associated pathology.
520 $a The contribution of γδ cells may be more critical in young mice due to the variable response of αβ cells at this time. The role of αβ cells in primary protection does not become critical until mice are greater than 40 days of age. In contrast, αβ cells are required for the development of immunity to re-challenge regardless of the age of the animal at primary infection.
520 $a γδ cells may mediate protection partially through an IFN-γ dependent mechanism. The susceptibility of 30 day old IFN-γ deficient mice is significantly less and of shorter duration than that of γδ cell-deficient mice however, demonstrating that IFN-γ production is not the sole mechanism of γδ cell action. Enhanced susceptibility of young B cell deficient mice suggests that γδ cells may also contribute to protection through interactions with other lymphocytes.
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