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Human T-cell lymphotropic virus type...

Mariner, Jennifer Marie.

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Human T-cell lymphotropic virus type I (HTLV-I) activates IL-15Ralpha expression via NF-kappaB and interferon regulatory elements.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	Human T-cell lymphotropic virus type I (HTLV-I) activates IL-15Ralpha expression via NF-kappaB and interferon regulatory elements./
Author:	Mariner, Jennifer Marie.
Description:	205 p.
Notes:	Directors: Thomas A. Waldmann; John Brady; Nazli Azimi.
Contained By:	Dissertation Abstracts International62-11B.
Subject:	Biology, Genetics. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3032759
ISBN:	0493452567

Human T-cell lymphotropic virus type I (HTLV-I) activates IL-15Ralpha expression via NF-kappaB and interferon regulatory elements.
Mariner, Jennifer Marie.

Human T-cell lymphotropic virus type I (HTLV-I) activates IL-15Ralpha expression via NF-kappaB and interferon regulatory elements. - 205 p.

Directors: Thomas A. Waldmann; John Brady; Nazli Azimi.

Thesis (Ph.D.)--The George Washington University, 2002.

Human T-cell Lymphotropic Virus Type-I (HTLV-I) is the causative agent of both Adult T Cell Leukemia (ATL) and HTLV-I Associated Myelopathy/Tropical Spastic Paraparesis (HAM/TSP). Interleukin-15 is a proliferative cytokine that is elevated in diseases caused by HTLV-I. In this dissertation, we demonstrated that interleukin 15 receptor alpha (IL-15Rα), the IL-15 specific binding receptor, mRNA levels were also elevated in HTLV-I infected cells. We also showed that IL-15Rα protein levels were elevated in HTLV-I infected cells using a newly developed polyclonal antibody directed against the receptor. We showed that transient HTLV-I Tax expression lead to increased IL-15Rα mRNA levels. In addition, by using a reporter construct that hears the human IL-15Rα promoter, we demonstrated that Tax expression increased activated IL-15Rα promoter activity. Using promoter deletion constructs and gel shift analysis, we defined a functional NF-κB binding motif in the human IL-15Rα promoter, suggesting that Tax activation of IL-15Rα is due, in part, to the induction of NF-κB. In addition, we demonstrated that an Interferon Regulatory Element (IRF-E) within the IL-15Rα promoter was also crucial for Tax-induced activation. This activation was mediated by IFR-4, an interferon regulatory factor elevated in ATL and HTLV-I infected cells These data indicate that IL-15Rα is transcriptionally regulated by the HTLV-I Tax protein through the action of NF-κB and IRF-4. These findings suggest a role for IL-15Rα in aberrant T cell proliferation observed in HTLV-I associated diseases.

ISBN: 0493452567Subjects--Topical Terms:

1017730
Biology, Genetics.

Human T-cell lymphotropic virus type I (HTLV-I) activates IL-15Ralpha expression via NF-kappaB and interferon regulatory elements.
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100 1 $a Mariner, Jennifer Marie. $3 1250757
245 1 0 $a Human T-cell lymphotropic virus type I (HTLV-I) activates IL-15Ralpha expression via NF-kappaB and interferon regulatory elements.
300 $a 205 p.
500 $a Directors: Thomas A. Waldmann; John Brady; Nazli Azimi.
500 $a Source: Dissertation Abstracts International, Volume: 62-11, Section: B, page: 5022.
502 $a Thesis (Ph.D.)--The George Washington University, 2002.
520 $a Human T-cell Lymphotropic Virus Type-I (HTLV-I) is the causative agent of both Adult T Cell Leukemia (ATL) and HTLV-I Associated Myelopathy/Tropical Spastic Paraparesis (HAM/TSP). Interleukin-15 is a proliferative cytokine that is elevated in diseases caused by HTLV-I. In this dissertation, we demonstrated that interleukin 15 receptor alpha (IL-15Rα), the IL-15 specific binding receptor, mRNA levels were also elevated in HTLV-I infected cells. We also showed that IL-15Rα protein levels were elevated in HTLV-I infected cells using a newly developed polyclonal antibody directed against the receptor. We showed that transient HTLV-I Tax expression lead to increased IL-15Rα mRNA levels. In addition, by using a reporter construct that hears the human IL-15Rα promoter, we demonstrated that Tax expression increased activated IL-15Rα promoter activity. Using promoter deletion constructs and gel shift analysis, we defined a functional NF-κB binding motif in the human IL-15Rα promoter, suggesting that Tax activation of IL-15Rα is due, in part, to the induction of NF-κB. In addition, we demonstrated that an Interferon Regulatory Element (IRF-E) within the IL-15Rα promoter was also crucial for Tax-induced activation. This activation was mediated by IFR-4, an interferon regulatory factor elevated in ATL and HTLV-I infected cells These data indicate that IL-15Rα is transcriptionally regulated by the HTLV-I Tax protein through the action of NF-κB and IRF-4. These findings suggest a role for IL-15Rα in aberrant T cell proliferation observed in HTLV-I associated diseases.
590 $a School code: 0075.
650 4 $a Biology, Genetics. $3 1017730
650 4 $a Health Sciences, Immunology. $3 1017716
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