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EGF module-containing mucin-like hor...

Song, Helen.

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EGF module-containing mucin-like hormone receptor 2 and its role in human immune privilege.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	EGF module-containing mucin-like hormone receptor 2 and its role in human immune privilege./
作者:	Song, Helen.
面頁冊數:	61 p.
附註:	Source: Masters Abstracts International, Volume: 53-02.
Contained By:	Masters Abstracts International53-02(E).
標題:	Immunology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=1559624
ISBN:	9781321004250

EGF module-containing mucin-like hormone receptor 2 and its role in human immune privilege.
Song, Helen.

EGF module-containing mucin-like hormone receptor 2 and its role in human immune privilege. - 61 p.

Source: Masters Abstracts International, Volume: 53-02.

Thesis (M.S.)--Boston University, 2014.

This item is not available from ProQuest Dissertations & Theses.

Purpose: In the mouse, the macrophage adhesion G protein-coupled receptor (ad-GPCR) molecule, F4/80, is required for the development of regulatory T cells in two models of tolerance, the eye and gut. Since F4/80 is not expressed in humans, the purpose of this research is to determine the human analog of F4/80. F4/80 belongs to a novel family of Epidermal growth factor-seven transmembrane (EGF-TM7) molecules, which include the EGF module-containing mucin-like hormone receptor (EMR) molecules. In the human, EMR1 has sequential homology with F4/80 and EMR2 has shown immune suppressing function in tumor cells. Thus, we investigate the possible suppressor role of the EMR family in human ocular tolerance.

ISBN: 9781321004250Subjects--Topical Terms:

611031
Immunology.

EGF module-containing mucin-like hormone receptor 2 and its role in human immune privilege.
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100 1 $a Song, Helen. $3 3179287
245 1 0 $a EGF module-containing mucin-like hormone receptor 2 and its role in human immune privilege.
300 $a 61 p.
500 $a Source: Masters Abstracts International, Volume: 53-02.
500 $a Advisers: Theresa A. Davies; Joan E. Stein-Streilein.
502 $a Thesis (M.S.)--Boston University, 2014.
506 $a This item is not available from ProQuest Dissertations & Theses.
520 $a Purpose: In the mouse, the macrophage adhesion G protein-coupled receptor (ad-GPCR) molecule, F4/80, is required for the development of regulatory T cells in two models of tolerance, the eye and gut. Since F4/80 is not expressed in humans, the purpose of this research is to determine the human analog of F4/80. F4/80 belongs to a novel family of Epidermal growth factor-seven transmembrane (EGF-TM7) molecules, which include the EGF module-containing mucin-like hormone receptor (EMR) molecules. In the human, EMR1 has sequential homology with F4/80 and EMR2 has shown immune suppressing function in tumor cells. Thus, we investigate the possible suppressor role of the EMR family in human ocular tolerance.
520 $a Methods: Human peripheral blood mononuclear cells (huPBMC) were treated with porcine TGFbeta2 and LPS or an antigenic stimulant for at least six hours to generate tolerogenic antigen presenting cells (APC). Cells were characterized by flow cytometric analysis for expression of CD14, CD40, PDL1, ILT3, and EMR2. Later, T regulatory cells were generated by incubating tolerogenic APCs with autologous huPBMC for five to seven days. Post culture, the T cells were stained and characterized for expression of CD4, CD25, and FoxP3.
520 $a Results: Post treatment of huPBMC with TGFbeta2 and antigen, the resulting tolerogenic APCs expressed PDL1, ILT3, and EMR2. CD40 remained unchanged and CD14 was constitutively expressed. Post five to seven day culture, tolerogenic APCs treated with TGFbeta2 increased the CD4+ CD25+ FoxP3+ lymphocyte populations.
520 $a Conclusions: The upregulation of EMR2 on human tolerogenic APCs suggests that EMR2 may have a role in inducing tolerance in humans. Much like its mouse counterpart, F4/80, EMR2 is an adhesion molecule that may facilitate the induction of naive T lymphocytes to regulatory T lymphocytes. Once the F4/80 analog is established for humans, novel therapies may be developed to interfere or encourage signaling in the treatment of tumors or immune inflammatory diseases, respectively.
590 $a School code: 0017.
650 4 $a Immunology. $3 611031
650 4 $a Ophthalmology. $3 862704
690 $a 0982
690 $a 0381
710 2 $a Boston University. $b Medical Sciences GMS. $3 2103826
773 0 $t Masters Abstracts International $g 53-02(E).
790 $a 0017
791 $a M.S.
792 $a 2014
793 $a English
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=1559624