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The Role of the Aryl Hydrocarbon Rec...

O'Driscoll, Chelsea A.

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The Role of the Aryl Hydrocarbon Receptor in Atmospheric Particulate Matter-Mediated Autoimmunity.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	The Role of the Aryl Hydrocarbon Receptor in Atmospheric Particulate Matter-Mediated Autoimmunity./
作者:	O'Driscoll, Chelsea A.
出版者:	Ann Arbor : ProQuest Dissertations & Theses, : 2018,
面頁冊數:	309 p.
附註:	Source: Dissertations Abstracts International, Volume: 81-05, Section: B.
Contained By:	Dissertations Abstracts International81-05B.
標題:	Toxicology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=10974171
ISBN:	9781392697740

The Role of the Aryl Hydrocarbon Receptor in Atmospheric Particulate Matter-Mediated Autoimmunity.
O'Driscoll, Chelsea A.

The Role of the Aryl Hydrocarbon Receptor in Atmospheric Particulate Matter-Mediated Autoimmunity. - Ann Arbor : ProQuest Dissertations & Theses, 2018 - 309 p.

Source: Dissertations Abstracts International, Volume: 81-05, Section: B.

Thesis (Ph.D.)--The University of Wisconsin - Madison, 2018.

This item must not be sold to any third party vendors.

In recent years, air pollution has emerged as a major risk factor for disease and death worldwide. These increases in air pollution have occurred concurrently with increases in incidence and prevalence of autoimmune disease. Currently there are over 80 recognized autoimmune diseases and genetic predispositions account for less than half of these leaving environmental factors as a major contributor. Epidemiologic data strongly suggest that exposure to air pollution, specifically atmospheric particulate matter (PM), aggravates autoimmune diseases. PM is a component of air pollution and is the largest environmental risk factor for premature death worldwide. PM is a complex heterogenous mixture composed of several different constituents including organic compounds such as polycyclic aromatic hydrocarbons (PAHs) and dioxins, among others. The chemically-extracted organic fraction (OF) of PM retains the organic compounds, including PAHs and dioxins, but eliminates everything else. The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that responds to both endogenous and exogenous ligands, including toxicants such as PAHs and dioxins found in PM, and activates cytochrome P450 (CYP) enzymes. The AHR has been shown to be crucial in the balance of regulatory and effector T cell differentiation and function both in vitro and in vivo using murine models of autoimmune disease. The overarching hypothesis of this body of work is that PAHs present in intact PM and its chemically-extracted OF alter T cell differentiation via the AHR and change autoimmune disease status. Chapter 1 reviewed the potential role of AHR in PM-mediated autoimmune disease, identifying immune roles the receptor may play in modulating disease. Chapter 2 aimed to identify the component present in PM that activates the AHR and worsens autoimmune disease using two diesel exhaust particles (DEPs). Chapter 3 focused on identifying potential mechanisms and therapeutic targets of PM-mediated autoimmune disease using an ambient urban dust particle. Chapter 4 aimed to identify immune cell types that exposure to the chemically extracted OF alters, leading to regulatory or inflammatory responses. Chapter 5 focused on understanding whether all PM of the same size alter T cell differentiation and activate the AHR to the same extent and thus should be regulated the same. Chapter 6 provides a summary of the findings and conclusions that can be drawn from all of the data as well as future directions for this work.

ISBN: 9781392697740Subjects--Topical Terms:

556884
Toxicology.
Subjects--Index Terms:

Aryl hydrocarbon receptor

The Role of the Aryl Hydrocarbon Receptor in Atmospheric Particulate Matter-Mediated Autoimmunity.
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300 $a 309 p.
500 $a Source: Dissertations Abstracts International, Volume: 81-05, Section: B.
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520 $a In recent years, air pollution has emerged as a major risk factor for disease and death worldwide. These increases in air pollution have occurred concurrently with increases in incidence and prevalence of autoimmune disease. Currently there are over 80 recognized autoimmune diseases and genetic predispositions account for less than half of these leaving environmental factors as a major contributor. Epidemiologic data strongly suggest that exposure to air pollution, specifically atmospheric particulate matter (PM), aggravates autoimmune diseases. PM is a component of air pollution and is the largest environmental risk factor for premature death worldwide. PM is a complex heterogenous mixture composed of several different constituents including organic compounds such as polycyclic aromatic hydrocarbons (PAHs) and dioxins, among others. The chemically-extracted organic fraction (OF) of PM retains the organic compounds, including PAHs and dioxins, but eliminates everything else. The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that responds to both endogenous and exogenous ligands, including toxicants such as PAHs and dioxins found in PM, and activates cytochrome P450 (CYP) enzymes. The AHR has been shown to be crucial in the balance of regulatory and effector T cell differentiation and function both in vitro and in vivo using murine models of autoimmune disease. The overarching hypothesis of this body of work is that PAHs present in intact PM and its chemically-extracted OF alter T cell differentiation via the AHR and change autoimmune disease status. Chapter 1 reviewed the potential role of AHR in PM-mediated autoimmune disease, identifying immune roles the receptor may play in modulating disease. Chapter 2 aimed to identify the component present in PM that activates the AHR and worsens autoimmune disease using two diesel exhaust particles (DEPs). Chapter 3 focused on identifying potential mechanisms and therapeutic targets of PM-mediated autoimmune disease using an ambient urban dust particle. Chapter 4 aimed to identify immune cell types that exposure to the chemically extracted OF alters, leading to regulatory or inflammatory responses. Chapter 5 focused on understanding whether all PM of the same size alter T cell differentiation and activate the AHR to the same extent and thus should be regulated the same. Chapter 6 provides a summary of the findings and conclusions that can be drawn from all of the data as well as future directions for this work.
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653 $a Autoimmunity
653 $a Dendritic cells
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