東華大學圖書館 |

Language: English

Help

回圖書館首頁

手機版館藏查詢

Back

Switch To: Labeled | MARC Mode | ISBD

CD24 in T lymphocyte homeostatic pro...

Li, Ou.

Linked to FindBook

Google Book

Amazon

博客來

CD24 in T lymphocyte homeostatic proliferation and autoimmune disease.

Record Type:	Electronic resources : Monograph/item
Title/Author:	CD24 in T lymphocyte homeostatic proliferation and autoimmune disease./
Author:	Li, Ou.
Description:	146 p.
Notes:	Source: Dissertation Abstracts International, Volume: 66-06, Section: B, page: 3044.
Contained By:	Dissertation Abstracts International66-06B.
Subject:	Health Sciences, Immunology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3180646
ISBN:	0542210169

CD24 in T lymphocyte homeostatic proliferation and autoimmune disease.
Li, Ou.

CD24 in T lymphocyte homeostatic proliferation and autoimmune disease. - 146 p.

Source: Dissertation Abstracts International, Volume: 66-06, Section: B, page: 3044.

Thesis (Ph.D.)--The Ohio State University, 2005.

In this thesis, we show that CD24 can regulate naive T cell homeostatic proliferation and autoimmune disease. The activation of T lymphocyte requires two signals from antigen presenting cells, peptide and self-MHC complex to TCR and co stimulatory signals. CD24, a glycosyl-phosphatidylinositol (GPI) arched glycoprotein, is an important co-stimulatory molecule. Although it is not essential for induction of T cell response, CD24 is required to express on T cells and for the induction of experimental autoimmune encephalomyelitis (EAE), an animal model for multiple sclerosis (MS). Here, we show that CD24 is essential for local clonal expansion and persistence of T cells after their migration into the CNS, and that expression of CD24 on either hematopoietic cells or non-hematopoietic antigen-presenting cells in the recipient is sufficient to confer susceptibility to EAE. At the same time, it is well established that T lymphocytes undergo homeostatic proliferation in lymphopenic environment. The homeostatic proliferation requires recognition of major histocompatibility complex on the host. Recent studies have demonstrated that co-stimulation, mediated by CD28, 4-1BB, and CD40, is not required for T cell homeostatic proliferation. Here, we report that T cells from mice with a targeted mutation of CD24 have a remarkably reduced rate of proliferation when adoptively transferred into syngeneic lymphopenic hosts. The reduced proliferation cannot be attributed to abnormal survival and homing properties of the CD24-deficient T cells. T cell proliferation in allogeneic hosts is less affected by this mutation. Thus, although distinct co-stimulatory molecules are involved in antigen-driven proliferation and homeostatic proliferation, both processes can be modulated by co-stimulatory molecules. Surprisingly, in the lymphopenic CD24-deficient mice, T cells launch an uncontrollable proliferation that results in rapid death of the recipient mice. The dividing T cells have the phenotypes similar to those activated by cognate antigens. In addition, the CD24-deficient DC have superior capacity to drive homeostatic proliferation of the syngeneic cells. Thus, our data demonstrate that CD24 expressed on the host antigen-presenting cells limits T cell response to homeostatic cue and prevents fatal damage associated with the uncontrolled homeostatic proliferation. Taken together, in this thesis, we demonstrate that although CD24 is not essential for the induction of T cell response, it can regulate T cell homeostatic proliferation and its function in autoimmune disease.

ISBN: 0542210169Subjects--Topical Terms:

1017716
Health Sciences, Immunology.

CD24 in T lymphocyte homeostatic proliferation and autoimmune disease.
LDR:03477nmm 2200289 4500 001 1815120
005 20060613121910.5
008 130610s2005 eng d
020 $a 0542210169
035 $a (UnM)AAI3180646
035 $a AAI3180646
040 $a UnM $c UnM
100 1 $a Li, Ou. $3 1904557
245 1 0 $a CD24 in T lymphocyte homeostatic proliferation and autoimmune disease.
300 $a 146 p.
500 $a Source: Dissertation Abstracts International, Volume: 66-06, Section: B, page: 3044.
500 $a Adviser: Yang Liu.
502 $a Thesis (Ph.D.)--The Ohio State University, 2005.
520 $a In this thesis, we show that CD24 can regulate naive T cell homeostatic proliferation and autoimmune disease. The activation of T lymphocyte requires two signals from antigen presenting cells, peptide and self-MHC complex to TCR and co stimulatory signals. CD24, a glycosyl-phosphatidylinositol (GPI) arched glycoprotein, is an important co-stimulatory molecule. Although it is not essential for induction of T cell response, CD24 is required to express on T cells and for the induction of experimental autoimmune encephalomyelitis (EAE), an animal model for multiple sclerosis (MS). Here, we show that CD24 is essential for local clonal expansion and persistence of T cells after their migration into the CNS, and that expression of CD24 on either hematopoietic cells or non-hematopoietic antigen-presenting cells in the recipient is sufficient to confer susceptibility to EAE. At the same time, it is well established that T lymphocytes undergo homeostatic proliferation in lymphopenic environment. The homeostatic proliferation requires recognition of major histocompatibility complex on the host. Recent studies have demonstrated that co-stimulation, mediated by CD28, 4-1BB, and CD40, is not required for T cell homeostatic proliferation. Here, we report that T cells from mice with a targeted mutation of CD24 have a remarkably reduced rate of proliferation when adoptively transferred into syngeneic lymphopenic hosts. The reduced proliferation cannot be attributed to abnormal survival and homing properties of the CD24-deficient T cells. T cell proliferation in allogeneic hosts is less affected by this mutation. Thus, although distinct co-stimulatory molecules are involved in antigen-driven proliferation and homeostatic proliferation, both processes can be modulated by co-stimulatory molecules. Surprisingly, in the lymphopenic CD24-deficient mice, T cells launch an uncontrollable proliferation that results in rapid death of the recipient mice. The dividing T cells have the phenotypes similar to those activated by cognate antigens. In addition, the CD24-deficient DC have superior capacity to drive homeostatic proliferation of the syngeneic cells. Thus, our data demonstrate that CD24 expressed on the host antigen-presenting cells limits T cell response to homeostatic cue and prevents fatal damage associated with the uncontrolled homeostatic proliferation. Taken together, in this thesis, we demonstrate that although CD24 is not essential for the induction of T cell response, it can regulate T cell homeostatic proliferation and its function in autoimmune disease.
590 $a School code: 0168.
650 4 $a Health Sciences, Immunology. $3 1017716
650 4 $a Health Sciences, Pathology. $3 1017854
650 4 $a Biology, Cell. $3 1017686
690 $a 0982
690 $a 0571
690 $a 0379
710 2 0 $a The Ohio State University. $3 718944
773 0 $t Dissertation Abstracts International $g 66-06B.
790 1 0 $a Liu, Yang, $e advisor
790 $a 0168
791 $a Ph.D.
792 $a 2005
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3180646