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

How B cells shape the immune respons...

Yeshiva University.

FindBook

Google Book

Amazon

博客來

How B cells shape the immune response against Mycobacterium tuberculosis.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	How B cells shape the immune response against Mycobacterium tuberculosis./
作者:	Maglione, Paul Joseph.
面頁冊數:	195 p.
附註:	Adviser: John Chan.
Contained By:	Dissertation Abstracts International68-09B.
標題:	Biology, Microbiology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3285397
ISBN:	9780549274834

How B cells shape the immune response against Mycobacterium tuberculosis.
Maglione, Paul Joseph.

How B cells shape the immune response against Mycobacterium tuberculosis. - 195 p.

Adviser: John Chan.

Thesis (Ph.D.)--Yeshiva University, 2008.

Extensive work illustrating the importance of cellular immune mechanisms for protection against Mycobacterium tuberculosis has largely relegated B cell biology to an afterthought within tuberculosis (TB) host defense. However, recent studies have illuminated how B lymphocytes, through a variety of interactions with the cellular immune response, play previously underappreciated roles in host defense against intracellular pathogens. Consequently, we hypothesized that B cells and the humoral response influence host defense against M. tuberculosis by regulating cellular immunity.

ISBN: 9780549274834Subjects--Topical Terms:

1017734
Biology, Microbiology.

How B cells shape the immune response against Mycobacterium tuberculosis.
LDR:03523nam 2200301 a 45 001 852057
005 20100629
008 100629s2008 ||||||||||||||||| ||eng d
020 $a 9780549274834
035 $a (UMI)AAI3285397
035 $a AAI3285397
040 $a UMI $c UMI
100 1 $a Maglione, Paul Joseph. $3 1017733
245 1 0 $a How B cells shape the immune response against Mycobacterium tuberculosis.
300 $a 195 p.
500 $a Adviser: John Chan.
500 $a Source: Dissertation Abstracts International, Volume: 68-09, Section: B, page: 5724.
502 $a Thesis (Ph.D.)--Yeshiva University, 2008.
520 $a Extensive work illustrating the importance of cellular immune mechanisms for protection against Mycobacterium tuberculosis has largely relegated B cell biology to an afterthought within tuberculosis (TB) host defense. However, recent studies have illuminated how B lymphocytes, through a variety of interactions with the cellular immune response, play previously underappreciated roles in host defense against intracellular pathogens. Consequently, we hypothesized that B cells and the humoral response influence host defense against M. tuberculosis by regulating cellular immunity.
520 $a Using flow cytometry and immunohistochemistry, we observed that B cells form profound pulmonary lymphoid aggregates during TB that express peanut agglutinin and GL7, two markers of germinal center B cells, in conjunction with CXCR5, a chemokine receptor that mediates the organization of B cells in lymphoid follicles. Further demonstrating characteristics of lymphoid tissue B cells, these pulmonary lymphocytes migrate in response to the lymphoid-associated chemokine CXCL13. We found that B cells both enhance mycobacterial containment and limit resultant immunopathology. Adoptive transfer of B cells complements the phenotypes of B cell-deficient mice without local residence of the transferred lymphocytes in the lungs, demonstrating that B cells mediate protective effects in an endocrine manner.
520 $a Fcgamma receptors regulate immunity by engaging immunoglobulins produced by B cells. C57BL/6 mice deficient in the inhibitory Fcgamma receptor, FcgammaRIIB, manifested enhanced mycobacterial containment and diminished immunopathology. These findings corresponded with increased IFN-gamma-producing CD4+ T cells as well as elevated expression of MHC II and B7 co-stimulatory molecules in the lungs. Upon M. tuberculosis infection and immune complex engagement, RIIB -/- macrophages produced more Th1-promoting IL-12p40. These data strongly suggest that FcgammaRIIB engagement can dampen the TB Th1 response by attenuating IL-12 production and/or activation of antigen presenting cells. Conversely, C57BL/6 mice lacking the gamma-chain shared by activating Fcgamma receptors had enhanced susceptibility and exacerbated immunopathology upon M. tuberculosis challenge, associated with increased production of the immunosuppressive cytokine IL-10. Thus, engagement of distinct Fcgamma receptors can divergently affect cytokine production and susceptibility during M. tuberculosis infection. Altering the endocrine immune regulation mediated by antibodies and Fcgamma receptors may provide novel means of enhancing immunity against M. tuberculosis.
590 $a School code: 0266.
650 4 $a Biology, Microbiology. $3 1017734
650 4 $a Health Sciences, Immunology. $3 1017716
690 $a 0410
690 $a 0982
710 2 $a Yeshiva University. $3 1017732
773 0 $t Dissertation Abstracts International $g 68-09B.
790 $a 0266
790 1 0 $a Chan, John, $e advisor
791 $a Ph.D.
792 $a 2008
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3285397