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New strategies to accelerate pathoge...

Jin, Feng.

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New strategies to accelerate pathogenic antibody elimination for the treatment of humoral autoimmune conditions.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	New strategies to accelerate pathogenic antibody elimination for the treatment of humoral autoimmune conditions./
作者:	Jin, Feng.
面頁冊數:	285 p.
附註:	Adviser: Joseph P. Balthasar.
Contained By:	Dissertation Abstracts International67-04B.
標題:	Health Sciences, Immunology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3213886
ISBN:	9780542630897

New strategies to accelerate pathogenic antibody elimination for the treatment of humoral autoimmune conditions.
Jin, Feng.

New strategies to accelerate pathogenic antibody elimination for the treatment of humoral autoimmune conditions. - 285 p.

Adviser: Joseph P. Balthasar.

Thesis (Ph.D.)--State University of New York at Buffalo, 2006.

Autoimmune diseases represent a host of more than 80 clinical conditions that are provoked by the attacks of immune system against self organs, tissues, and cells. Many of these diseases are humoral in nature, where pathogenic autoantibodies are mediating the disease progression (e.g. immune thrombocytope nic purpura, ITP). Therapeutic strategies that are aimed to reduce pathogenic antibody concentrations may dramatically ameliorate the autoimmune conditions. The purpose of this research was to develop new approaches to accelerate the elimination of pathogenic autoantibodies and test these approaches in animal models of autoimmunity (e.g. ITP). It is hypothesized that by functionally inhibiting FcRn (neonatal Fc receptor), a receptor responsible for protecting IgG from catabolism, the elimination of pathogenic anti-platelet antibodies may be significantly enhanced. Consequently the anti platelet antibody-induced thrombocytopenia may be attenuated.

ISBN: 9780542630897Subjects--Topical Terms:

1017716
Health Sciences, Immunology.

New strategies to accelerate pathogenic antibody elimination for the treatment of humoral autoimmune conditions.
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245 1 0 $a New strategies to accelerate pathogenic antibody elimination for the treatment of humoral autoimmune conditions.
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520 $a Autoimmune diseases represent a host of more than 80 clinical conditions that are provoked by the attacks of immune system against self organs, tissues, and cells. Many of these diseases are humoral in nature, where pathogenic autoantibodies are mediating the disease progression (e.g. immune thrombocytope nic purpura, ITP). Therapeutic strategies that are aimed to reduce pathogenic antibody concentrations may dramatically ameliorate the autoimmune conditions. The purpose of this research was to develop new approaches to accelerate the elimination of pathogenic autoantibodies and test these approaches in animal models of autoimmunity (e.g. ITP). It is hypothesized that by functionally inhibiting FcRn (neonatal Fc receptor), a receptor responsible for protecting IgG from catabolism, the elimination of pathogenic anti-platelet antibodies may be significantly enhanced. Consequently the anti platelet antibody-induced thrombocytopenia may be attenuated.
520 $a Two new strategies have been developed to inhibit FcRn. The first strategy is high dose monoclonal antibodies. Administration of monoclonal anti-methotrexate antibody (AMI) at 1 g/kg successfully increased the elimination of anti-platelet antibody (7E3) and attenuated thrombocytopenia induced by 7E3 in a rat model of ITP. Pharmacokinetic/pharmacodynamic modeling was used to assess the importance of the effect of AMI on 7E3 pharmacokinetics relative to its overall effect on thrombocytopenia. The modeling results suggest that &sim;12% of the overall effect of AMI on thrombocytopenia can be explained by AMI-induced increase of 7E3 elimination. Anti-FcRn antibodies represent the second strategy for functional inhibition of FcRn. Administration of a monoclonal anti-FcRn antibody, 1G3, significantly increased the elimination of anti-platelet antibody (MWReg30) and attenuated MWReg30-induced thrombocytopenia in a murine model of chronic ITP. Pharmacokinetic/pharmacodynamic modeling results suggest that, compared to high dose intravenous immunoglobulin therapy, of which the dose level is typically 1-2 g/kg, 1G3 could elicit similar effect on anti-platelet antibody elimination at doses that are almost 50-fold lower. Pharmacokinetic/pharmacodynamic modeling suggests that bolus injection at 30 mg/kg may be the desirable dosing protocol for the treatment of chronic ITP in the mouse ITP model. Finally, polyclonal and monoclonal anti human FcRn antibodies were developed and characterized. (Abstract shortened by UMI.)
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