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Computational Methods and Epidemiologic Approaches for Revealing the Etiology of Autoimmune Diseases

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서명/저자사항Computational Methods and Epidemiologic Approaches for Revealing the Etiology of Autoimmune Diseases.
개인저자Rhead, Brooke.
단체저자명University of California, Berkeley. Bioinformatics & Computational Biology.
발행사항[S.l.]: University of California, Berkeley., 2019.
발행사항Ann Arbor: ProQuest Dissertations & Theses, 2019.
형태사항109 p.
기본자료 저록Dissertations Abstracts International 81-05B.
Dissertation Abstract International
ISBN9781392825402
학위논문주기Thesis (Ph.D.)--University of California, Berkeley, 2019.
일반주기 Source: Dissertations Abstracts International, Volume: 81-05, Section: B.
Includes supplementary digital materials.
Advisor: Barcellos, Lisa F.
이용제한사항This item must not be sold to any third party vendors.
요약Autoimmune diseases, in which normal tissues are inappropriately attacked by the immune system, are complex diseases driven by a combination of genetic and environmental factors. Most are chronic inflammatory diseases with some treatments available but no known cures, and the disease mechanisms are not completely understood. Epigenetic factors, such as DNA methylation and microRNAs, are affected by genetic and environmental exposures and in turn affect gene expression and thus may play a role in autoimmune disease pathogenesis. In this dissertation, I employ a combination of computational, bioinformatic, statistical, and epidemiologic methods to study the role of epigenetics in autoimmune diseases in humans, and to characterize inflammatory changes in human cell lines.Chapter one introduces some complexities of studying autoimmune diseases in humans and introduces concepts of epigenetics. Chapter two shows that naive T cells from rheumatoid arthritis patients share DNA methylation sites with fibroblast-like synoviocytes, cells that line joints and are involved in joint inflammation. Chapter three shows that there are differences in DNA methylation in CD4+ and CD8+ T cells from multiple sclerosis patients compared to cells from healthy controls. Chapter four uses genome-wide association study results to implicate specific microRNAs and tissues in pediatric-onset multiple sclerosis. Chapter five shows that the inflammatory cytokine tumor necrosis factor alpha drives DNA methylation and transcriptional changes and activates autoimmune disease genes in endothelial cells. Chapter six is a summary of conclusions and key findings.
일반주제명Genetics.
Epidemiology.
Biostatistics.
언어영어
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