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Investigating B cell and T cell Cogn...

Giles, Josephine Ruth.

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Investigating B cell and T cell Cognate Interactions in Systemic Lupus Erythematosus: A Novel System for the Study of Lupus Antigen-Specific T cells.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Investigating B cell and T cell Cognate Interactions in Systemic Lupus Erythematosus: A Novel System for the Study of Lupus Antigen-Specific T cells./
作者:	Giles, Josephine Ruth.
面頁冊數:	215 p.
附註:	Source: Dissertation Abstracts International, Volume: 76-11(E), Section: B.
Contained By:	Dissertation Abstracts International76-11B(E).
標題:	Immunology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3663439
ISBN:	9781321928310

Investigating B cell and T cell Cognate Interactions in Systemic Lupus Erythematosus: A Novel System for the Study of Lupus Antigen-Specific T cells.
Giles, Josephine Ruth.

Investigating B cell and T cell Cognate Interactions in Systemic Lupus Erythematosus: A Novel System for the Study of Lupus Antigen-Specific T cells. - 215 p.

Source: Dissertation Abstracts International, Volume: 76-11(E), Section: B.

Thesis (Ph.D.)--Yale University, 2015.

Systemic lupus erythematosus (SLE) is a debilitating disease caused by a misdirected immune response towards self tissues that results from a combination of allelic risk factors, environmental influences, and stochastic events. While the various permutations of these components can be distinct for individual patients, the interactions between autoreactive B cells and T cells are likely to be a common critical force that drives disease pathogenesis.

ISBN: 9781321928310Subjects--Topical Terms:

611031
Immunology.

Investigating B cell and T cell Cognate Interactions in Systemic Lupus Erythematosus: A Novel System for the Study of Lupus Antigen-Specific T cells.
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245 1 0 $a Investigating B cell and T cell Cognate Interactions in Systemic Lupus Erythematosus: A Novel System for the Study of Lupus Antigen-Specific T cells.
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500 $a Adviser: Mark J. Shlomchik.
502 $a Thesis (Ph.D.)--Yale University, 2015.
520 $a Systemic lupus erythematosus (SLE) is a debilitating disease caused by a misdirected immune response towards self tissues that results from a combination of allelic risk factors, environmental influences, and stochastic events. While the various permutations of these components can be distinct for individual patients, the interactions between autoreactive B cells and T cells are likely to be a common critical force that drives disease pathogenesis.
520 $a Previous work has demonstrated that B cells have multiple antibody-dependent and -independent roles in SLE. Studies using B cell deficient lupus-prone mice suggest that B cells may be critical antigen presenting cells (ADCs) for initiating the T cell response, but this has never been directly tested. By specifically deleting MHC class II (MHCII) on B cells, we demonstrated that B cells do play a non-redundant role in activating T cells in a spontaneous, polygenic murine model of lupus. We also show that the ability of B cells to interact with T cells in a cognate manner significantly enhanced B cell proliferation and differentiation into antibody forming cells (AFCs). In the absence of these antigen-specific interactions, clinical disease was significantly reduced.
520 $a Understanding the mechanistic detail of these interactions has been significantly hampered by the absence of a lupus antigen-specific T cell model. This is in large part because identifying T cells that recognize ubiquitous self antigens has been extremely challenging. We developed a system to identify immune complex (IC)-specific T cells using rheumatoid factor (RF) B cells and autoantibodies which form spontaneous immune complexes. Since ICs are complex, undefined self antigens, they provided the opportunity to discover previously unknown T cell self antigens. Proteomic techniques and bioinformatic analysis identified several potential self antigens for these T cells, most of which were from ubiquitous nucleic acid-binding proteins.
520 $a We used one of these newly characterized autoreactive T cell clones to investigate cognate T cell-B cell interactions in response to lupus autoantigens. We found the IC-specific T cells significantly enhanced the RF B cell response to nucleic acid-reactive autoantibodies. In vitro, the cognate help provided by the IC-specific T cells alleviated the requirement of TLR signaling for the RF B cell proliferative response. In vivo, the presence of IC-specific T cells dramatically altered B cell differentiation, directing anti-chromatin stimulated-B cells from a plasmablast to a germinal center (GC) fate.
520 $a The work described here established a new method for identifying autoreactive T cells and discovering new T cell antigen relevant for systemic autoimmune disease.
590 $a School code: 0265.
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