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The function of the transcription fa...

Lugo-Villarino, Geanncarlo.

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The function of the transcription factor T-bet in dendritic cells.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	The function of the transcription factor T-bet in dendritic cells./
作者:	Lugo-Villarino, Geanncarlo.
面頁冊數:	156 p.
附註:	Source: Dissertation Abstracts International, Volume: 67-02, Section: B, page: 0796.
Contained By:	Dissertation Abstracts International67-02B.
標題:	Biology, Molecular. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3205927
ISBN:	9780542547164

The function of the transcription factor T-bet in dendritic cells.
Lugo-Villarino, Geanncarlo.

The function of the transcription factor T-bet in dendritic cells. - 156 p.

Source: Dissertation Abstracts International, Volume: 67-02, Section: B, page: 0796.

Thesis (Ph.D.)--Harvard University, 2006.

Dendritic cells (DCs) can elicit different immune responses characterized by the differentiation of two distinct lineages of effector CD4+ T helper (Th) cells: Th1 and Th2. Th1 cells produce IFNgamma to orchestrate cell-mediated responses against intracellular pathogens, whereas Th2 cells produce IL-4 to promote humoral responses to eradicate extracellular pathogens. T-bet is a transcription factor that governs the IFNgamma gene expression and T helper differentiation. As a consequence, T-bet-/- exhibited an impaired type-1 immune response. Here we sought to determine if T-bet is a polarization factor that affects the ability of DCs to drive type-1 immunity.

ISBN: 9780542547164Subjects--Topical Terms:

1017719
Biology, Molecular.

The function of the transcription factor T-bet in dendritic cells.
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100 1 $a Lugo-Villarino, Geanncarlo. $3 1917872
245 1 4 $a The function of the transcription factor T-bet in dendritic cells.
300 $a 156 p.
500 $a Source: Dissertation Abstracts International, Volume: 67-02, Section: B, page: 0796.
500 $a Adviser: Laurie H. Glimcher.
502 $a Thesis (Ph.D.)--Harvard University, 2006.
520 $a Dendritic cells (DCs) can elicit different immune responses characterized by the differentiation of two distinct lineages of effector CD4+ T helper (Th) cells: Th1 and Th2. Th1 cells produce IFNgamma to orchestrate cell-mediated responses against intracellular pathogens, whereas Th2 cells produce IL-4 to promote humoral responses to eradicate extracellular pathogens. T-bet is a transcription factor that governs the IFNgamma gene expression and T helper differentiation. As a consequence, T-bet-/- exhibited an impaired type-1 immune response. Here we sought to determine if T-bet is a polarization factor that affects the ability of DCs to drive type-1 immunity.
520 $a We initially demonstrated that T-bet is essential for the optimal production of IFNgamma by DCs. More importantly, T-bet-/- DCs were impaired in their ability to activate the Th1 program of adoptively transferred antigen-specific T cells. Subsequently, we investigated the role for T-bet in DCs in modulating innate immunity against intracellular pathogens. Rag2-/- mice, devoid of lymphocytes, were able to survive a lethal challenge with L. Monocytogenes when treated with CpG-ODN. Strikingly, the CpG-ODN treatment failed to rescue Rag2-/- mice that also lacked T-bet (DKO). Since CpG-ODN is known to promote a Th1 environment, we investigated its effects on T-bet-/- DCs. The transfer of CD11chi DCs from wildtype, but not from T-bet-/-, CpG ODN-treated mice rescued the DKO animals. Therefore, we concluded that T-bet expression in DCs is required for the adjuvant activity of CpG-ODN.
520 $a The equilibrium between Th1/Th2 dictates the eradication of microbes. However, when this balance is broken, it determines the susceptibility to diseases. We then examined the role for T-bet in DCs during inflammatory arthritis. T-bet-/- mice had reduced joint inflammation upon collagen antibody-induced arthritis (CAIA), while DKO mice were resistant to disease. Remarkably, adoptive transfer of activated wildtype DCs reconstituted CAIA inflammation in these mice. Based on these observations, we propose that an aberrant expression of T-bet in DCs influences the development of rheumatoid arthritis.
520 $a Altogether, the body of work described in this PhD dissertation provides evidence that DCs are another venue for T-bet to drive type-1 immunity. T-bet represents an essential transcription factor that tightly intermingles the innate and adaptive immune systems.
590 $a School code: 0084.
650 4 $a Biology, Molecular. $3 1017719
650 4 $a Biology, Microbiology. $3 1017734
650 4 $a Health Sciences, Immunology. $3 1017716
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710 2 0 $a Harvard University. $3 528741
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791 $a Ph.D.
792 $a 2006
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