東華大學圖書館 |

語系: 繁體中文

說明(常見問題)

回圖書館首頁

手機版館藏查詢

登入

回首頁

切換: 標籤 | MARC模式 | ISBD

A study in the loss of tolerance to ...

Harris, Geoffrey Stewart.

FindBook

Google Book

Amazon

博客來

A study in the loss of tolerance to a native serum protein.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	A study in the loss of tolerance to a native serum protein./
作者:	Harris, Geoffrey Stewart.
面頁冊數:	102 p.
附註:	Source: Dissertation Abstracts International, Volume: 65-06, Section: B, page: 2883.
Contained By:	Dissertation Abstracts International65-06B.
標題:	Health Sciences, Pathology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3137551
ISBN:	0496847252

A study in the loss of tolerance to a native serum protein.
Harris, Geoffrey Stewart.

A study in the loss of tolerance to a native serum protein. - 102 p.

Source: Dissertation Abstracts International, Volume: 65-06, Section: B, page: 2883.

Thesis (Ph.D.)--University of California, Davis, 2004.

The mammalian immune system is a complex system designed to maintain and restore health after encounters with foreign invading organisms. Besides this, it must also recognize and maintain tolerance to self tissues. The breakdown of the regulatory mechanisms leading to loss of tolerance and the development of autoimmune diseases are subjects of intense study. Few simple systems exist where a known instigator can reliably lead to loss of tolerance of a know target antigen.

ISBN: 0496847252Subjects--Topical Terms:

1017854
Health Sciences, Pathology.

A study in the loss of tolerance to a native serum protein.
LDR:04291nmm 2200337 4500 001 1851369
005 20051216110252.5
008 130614s2004 eng d
020 $a 0496847252
035 $a (UnM)AAI3137551
035 $a AAI3137551
040 $a UnM $c UnM
100 1 $a Harris, Geoffrey Stewart. $3 1939261
245 1 2 $a A study in the loss of tolerance to a native serum protein.
300 $a 102 p.
500 $a Source: Dissertation Abstracts International, Volume: 65-06, Section: B, page: 2883.
500 $a Chair: Jerry Powell.
502 $a Thesis (Ph.D.)--University of California, Davis, 2004.
520 $a The mammalian immune system is a complex system designed to maintain and restore health after encounters with foreign invading organisms. Besides this, it must also recognize and maintain tolerance to self tissues. The breakdown of the regulatory mechanisms leading to loss of tolerance and the development of autoimmune diseases are subjects of intense study. Few simple systems exist where a known instigator can reliably lead to loss of tolerance of a know target antigen.
520 $a Over the last several years, several hundred cases of acquired pure red cell aplasia (PRCA) have been discovered in patients receiving recombinant human erythropoietin (rhEPO). From the outset, it appeared that these cases were temporally related to rhEPO administration and that the cause was due to an immune response directed at both native and recombinant EPO. The development of acquired PRCA also occurs in other species treated with rhEPO but at a dramatically higher rate than the human population. This led to the idea that an animal model of acquired PRCA could be developed and studied to determine what factors are involved in the genesis of rhEPO-induced acquired PRCA as well as determine how it might be treated.
520 $a Chapter one provides an overview of both the development of rhEPO-induced acquired PRCA as well as an overview of how both normal and abnormal immune responses develop. It also highlights several areas of immunologic function that may be important in the development of this disease.
520 $a Chapter two explores the development of a mouse model of rhEPO-induced acquired PRCA. The data suggest that in mice there is a genetic basis for the development of rhEPO-induced acquired PRCA. The basis of this genetic predisposition is unknown, but speculated about. The data also suggest that the presentation of the disease is not solely due to genetics and that downstream events in the activation of a humoral immune response are also important in the development of the disease.
520 $a Chapter three explores the necessity of IgG and B cells in the development of rhEPO-induced acquired PRCA. Using knock out mice incapable of making B cells on the same background strain that is susceptible to the development of rhEPO-induced acquired PRCA, the data show that this immunological defect is sufficient to prevent the development of the disease. Since B cell depletion strategies are available in human medicine, it is hypothesized that this might be a reasonable intervention point to treat the development of rhEPO-induced acquired PRCA in humans.
520 $a Chapter four details the interaction between B cells and CD4+ T cells in the development of rhEPO-induced acquired PRCA. Using knock out mice with a defect in CD40L expression, the data show that costimulation provided by CD40L is essential to the development of the disease. However, the lack of CD40L is not sufficient to allow engraftment of the foreign protein. This is significant, as therapeutics designed to disrupt the interaction of CD40 and CD40L have been postulated as a possible way to induce tolerance to foreign proteins. This data would suggest that this is not the case for EPO using adeno-associated virus for the delivery system. This data also suggests that the molecular events that occur in B cells after CD40-CD40L ligation are essential for loss of tolerance to occur in this model.
590 $a School code: 0029.
650 4 $a Health Sciences, Pathology. $3 1017854
650 4 $a Health Sciences, Immunology. $3 1017716
690 $a 0571
690 $a 0982
710 2 0 $a University of California, Davis. $3 1018682
773 0 $t Dissertation Abstracts International $g 65-06B.
790 1 0 $a Powell, Jerry, $e advisor
790 $a 0029
791 $a Ph.D.
792 $a 2004
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3137551