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The role of type I interferons in T ...

Mangini, Alyson J.

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The role of type I interferons in T helper cell inflammatory responses in systemic lupus erythematosus.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	The role of type I interferons in T helper cell inflammatory responses in systemic lupus erythematosus./
作者:	Mangini, Alyson J.
面頁冊數:	235 p.
附註:	Source: Dissertation Abstracts International, Volume: 72-04, Section: B, page: 2021.
Contained By:	Dissertation Abstracts International72-04B.
標題:	Health Sciences, Pathology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3445696
ISBN:	9781124491486

The role of type I interferons in T helper cell inflammatory responses in systemic lupus erythematosus.
Mangini, Alyson J.

The role of type I interferons in T helper cell inflammatory responses in systemic lupus erythematosus. - 235 p.

Source: Dissertation Abstracts International, Volume: 72-04, Section: B, page: 2021.

Thesis (Ph.D.)--Boston University, 2011.

Type I interferons (IFNs) can mediate both positive and negative regulatory effects on inflammatory T helper (Th) cell function depending on the timing and duration of exposure. In systemic lupus erythematosus (SLE), the clinical and cellular manifestations of excessive production of IFN-alpha mark this cytokine as a key disease effector. Despite development of type I IFN-targeting therapeutics, the immunoregulatory activity of type I IFNs on Th cell responses in SLE is unknown. The goal of this research is to identify the role of type I IFNs in regulating inflammatory Th cell responses in SLE.

ISBN: 9781124491486Subjects--Topical Terms:

1017854
Health Sciences, Pathology.

The role of type I interferons in T helper cell inflammatory responses in systemic lupus erythematosus.
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245 1 4 $a The role of type I interferons in T helper cell inflammatory responses in systemic lupus erythematosus.
300 $a 235 p.
500 $a Source: Dissertation Abstracts International, Volume: 72-04, Section: B, page: 2021.
500 $a Adviser: David H. Sherr.
502 $a Thesis (Ph.D.)--Boston University, 2011.
520 $a Type I interferons (IFNs) can mediate both positive and negative regulatory effects on inflammatory T helper (Th) cell function depending on the timing and duration of exposure. In systemic lupus erythematosus (SLE), the clinical and cellular manifestations of excessive production of IFN-alpha mark this cytokine as a key disease effector. Despite development of type I IFN-targeting therapeutics, the immunoregulatory activity of type I IFNs on Th cell responses in SLE is unknown. The goal of this research is to identify the role of type I IFNs in regulating inflammatory Th cell responses in SLE.
520 $a Our results indicate that in some SLE patients circulating type I IFNs play a protective role by negatively regulating inflammatory Th cell responses. Specifically, both circulating IgG autoimmune complexes and endogenous IFN-alpha in SLE patient sera were shown to block the effector functions of Th1 and Th17 cells within healthy donor peripheral blood mononuclear cells by down-regulating secretion of inflammatory cytokines, IFN-gamma, interleukin (IL)-17, lymphotoxin (LT) and tumor necrosis factor alpha (TNF-alpha), while elevating anti-inflammatory, IL-10 secretion. The significant correlation between this anti-inflammatory effect and the presence within sera of specific anti-dsDNA, anti-RNP and anti-Sm autoantibodies indicates a potential disease biomarker to identify patients in which therapies that target type I IFN activity could potentiate Th cell IFN-gamma/1L-17-mediated autoimmune inflammation.
520 $a Results indicate that the absence of type I IFN signaling in genetic type I IFN receptor (IFNAR) deficient mice inhibits the onset/progression of autoimmune disease in the gld.apoE-/- murine model of lupus-like autoimmune disease and associated atherosclerosis. Specifically, compared to gld.apoE-/- mice, gld.apoE-/- .ifnar-/- mice had decreased splenomegaly, lymphadenopathy, lymphoproliferation, hypergammaglobinemia, and serum anti-dsDNA levels, and markedly delayed development of glomerulonephritis. In contrast, type I IFN deficiency promoted atherosclerosis as indicated by an increase in aortic lesions and tissue endothelin-1 expression.
520 $a Collectively these results suggest a multifaceted role for type I IFNs in SLE. They indicate a potential beneficial effect of Type I IFN targeting early in disease, while suggesting the potential for deleterious effects if type I IFN blockade is initiated in patients with advanced disease involving substantial inflammatory Th cell activity and/or cardiovascular complications.
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650 4 $a Health Sciences, Immunology. $3 1017716
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773 0 $t Dissertation Abstracts International $g 72-04B.
790 1 0 $a Sherr, David H., $e advisor
790 $a 0017
791 $a Ph.D.
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