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Interferon-gamma regulates T-helper ...

Wensky, Allen K.

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Interferon-gamma regulates T-helper type 2 subpopulation development and site-specific inflammation in autoimmune encephalomyelitis.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Interferon-gamma regulates T-helper type 2 subpopulation development and site-specific inflammation in autoimmune encephalomyelitis./
作者:	Wensky, Allen K.
面頁冊數:	172 p.
附註:	Source: Dissertation Abstracts International, Volume: 63-12, Section: B, page: 5754.
Contained By:	Dissertation Abstracts International63-12B.
標題:	Health Sciences, Immunology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3075530
ISBN:	0493958339

Interferon-gamma regulates T-helper type 2 subpopulation development and site-specific inflammation in autoimmune encephalomyelitis.
Wensky, Allen K.

Interferon-gamma regulates T-helper type 2 subpopulation development and site-specific inflammation in autoimmune encephalomyelitis. - 172 p.

Source: Dissertation Abstracts International, Volume: 63-12, Section: B, page: 5754.

Thesis (Ph.D.)--New York University, 2003.

Experimental autoimmune encephalomyelitis (EAE), the murine model for multiple sclerosis (MS), is a demyelinating disease of the central nervous system (CNS) initiated by autoreactive CD4+ T cells. EAE is typically considered a T helper type 1 (Th1) disease but work from our lab utilizing T cell receptor (TCR) transgenic mice specific for a component of myelin has demonstrated that under certain circumstances disease can be induced by T helper type 2 (Th2) cells. We can further delineate specific Th2 subsets termed Th2 (IL-4 producing) and Th2Hi5 (IL-4 and IL-5 producing) which transfer two clinically distinct forms of disease. EAE typically presents with a progressive ascending paralysis (classical EAE), which develops upon transfer of Th1 and Th2 cells into lymphopenic hosts. Th2Hi5 cells, on the other hand, transfer EAE that produces a non-classical form of disease (non-classical EAE) characterized by a head tilt, progressing finally to a rotatory motion around a rostral-to-caudal axis. Consistent with the clinical signs of non-classical disease, we observe pronounced inflammation in the brainstem and cerebellum with marked eosinophilia.

ISBN: 0493958339Subjects--Topical Terms:

1017716
Health Sciences, Immunology.

Interferon-gamma regulates T-helper type 2 subpopulation development and site-specific inflammation in autoimmune encephalomyelitis.
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500 $a Adviser: Juan J. Lafaille.
502 $a Thesis (Ph.D.)--New York University, 2003.
520 $a Experimental autoimmune encephalomyelitis (EAE), the murine model for multiple sclerosis (MS), is a demyelinating disease of the central nervous system (CNS) initiated by autoreactive CD4+ T cells. EAE is typically considered a T helper type 1 (Th1) disease but work from our lab utilizing T cell receptor (TCR) transgenic mice specific for a component of myelin has demonstrated that under certain circumstances disease can be induced by T helper type 2 (Th2) cells. We can further delineate specific Th2 subsets termed Th2 (IL-4 producing) and Th2Hi5 (IL-4 and IL-5 producing) which transfer two clinically distinct forms of disease. EAE typically presents with a progressive ascending paralysis (classical EAE), which develops upon transfer of Th1 and Th2 cells into lymphopenic hosts. Th2Hi5 cells, on the other hand, transfer EAE that produces a non-classical form of disease (non-classical EAE) characterized by a head tilt, progressing finally to a rotatory motion around a rostral-to-caudal axis. Consistent with the clinical signs of non-classical disease, we observe pronounced inflammation in the brainstem and cerebellum with marked eosinophilia.
520 $a Previous work in our lab has established that transgenic mice crossed to RAG-1 knockout mice (T/R-) spontaneously develop classical EAE. When crossed to IFN-gamma knockout mice (T/R-gamma -), however, all mice develop spontaneous, non-classical EAE. Based on the Th2Hi5 phenotype and the pronounced eosinophilia observed in non-classical disease we crossed T/R-gamma- mice with IL-5 deficient mice (T/R-gamma -5-, which revealed that IL-5 and eosinophilia are dispensable for non-classical disease development. Furthermore, IFN-gamma knockout T cells skewed toward the Th1 phenotype still produced non-classical disease but now with a monocytic character. Since chemokines have been implicated in EAE pathogenesis, we analyzed chemokine and chemokine receptor expression on various cells and tissue to define molecules downstream of IFN-gamma that could potentially influence migration to particular locations in the CNS.
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