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Tumor immunosurveillance by natural ...

Venook, Rayna Takaki.

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Tumor immunosurveillance by natural killer cells.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Tumor immunosurveillance by natural killer cells./
作者:	Venook, Rayna Takaki.
面頁冊數:	82 p.
附註:	Source: Dissertation Abstracts International, Volume: 67-08, Section: B, page: 4242.
Contained By:	Dissertation Abstracts International67-08B.
標題:	Biology, Microbiology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3229275
ISBN:	9780542828973

Tumor immunosurveillance by natural killer cells.
Venook, Rayna Takaki.

Tumor immunosurveillance by natural killer cells. - 82 p.

Source: Dissertation Abstracts International, Volume: 67-08, Section: B, page: 4242.

Thesis (Ph.D.)--University of California, San Francisco, 2006.

Natural killer cells are an integral component of the innate immune response that can quickly detect and eliminate infected or transformed cells without requiring prior sensitization. It has been demonstrated that NK cells play an important role in tumor immunosurveillance; however, the mechanisms regulating NK cell anti-tumor activity are still not well defined. The work presented in this thesis examines the effects of E1A-mediated transformation, interleukin-2I (IL-21) treatment, and DAP 12-mediated signaling on NK cell-mediated tumor rejection.

ISBN: 9780542828973Subjects--Topical Terms:

1017734
Biology, Microbiology.

Tumor immunosurveillance by natural killer cells.
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520 $a Natural killer cells are an integral component of the innate immune response that can quickly detect and eliminate infected or transformed cells without requiring prior sensitization. It has been demonstrated that NK cells play an important role in tumor immunosurveillance; however, the mechanisms regulating NK cell anti-tumor activity are still not well defined. The work presented in this thesis examines the effects of E1A-mediated transformation, interleukin-2I (IL-21) treatment, and DAP 12-mediated signaling on NK cell-mediated tumor rejection.
520 $a The ability of human adenovirus serotype 5 E1A, a viral oncoprotein, to sensitize tumor cells to NK cell-mediated lysis has been well demonstrated; however, the mechanisms regulating this sensitivity were previously unknown. We demonstrated that transformation of select tumor cells by E1A up-regulated NKG2D ligand expression on the tumor cells and, thereby, sensitized the tumor cells to NKG2D-dependent NK cell-mediated cytolytic activity. This E1A-induced sensitivity to NKG2D-dependent NK cell cytolytic activity enhanced tumor rejection, and mice injected with E1A-transformed tumor cells remained tumor free at significantly higher tumor cells doses compared to mice that were injected with parental cells not expressing E1A.
520 $a Next, we demonstrated that NK cell-mediated tumor rejection is enhanced by IL-21 treatment. Mice treated with IL-21 rejected select tumor cells more efficiently, and they remained tumor-free longer than untreated control mice. Additionally, we demonstrated that the IL-21-enhanced tumor rejection by NK cells was mediated by the NKG2D pathway and did not require the presence of an adaptive immune system. Finally, we demonstrated that DAP12 is an adapter protein with dual functionality that can activate and inhibit NK cell effector functions. We observed that DAP12-deficient NK cells exhibit hyper-responsive cytolytic activity and cytokine production. Furthermore, in vivo, the absence of DAP12 enhanced NK cell-mediated tumor rejection; and DAP12-deficient mice rejected tumor cells more efficiently than wild-type mice. These findings were consistent with our previous observations demonstrating that the absence of DAP12 enhances myeloid effector functions.
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