The Biology of Dendritic Cells in the Context of Autoimmunity

Systemic lupus erythematosus (SLE) is a complex autoimmune disease that affects at least five million people worldwide. An increased expression of type I interferon (IFN) regulated genes is a hallmark of SLE, but the precise etiology of SLE initiation and flares is poorly understood. Because plasmacytoid dendritic cells (pDCs) are the primary type I IFN producers, their role in SLE has long been suspected, with murine pDC depletion models successfully delaying the progression of murine lupus-like disease. However, the mechanism behind how exactly how pDCs contribute to lupus autoimmunity is unknown, contributing to the current dearth lack of disease modifying treatments; current treatments only succeed in suppressing symptoms, and do not halt disease progression. In this study, we take a multifactorial approach to understanding the biology of pDCs in the context of lupus autoimmunity. Although the exact etiology of lupus is unknown, infections are an important environmental trigger for

Grantor dc:publisher

Temple University. Libraries

Year dc:date.issued

2019

Author dc:creator

• Qiu, Connie Claire

Advisor dc:contributor.advisor

• Gallucci, Stefania

Committee members dc:contributor.committeemember

• Caricchio, Roberto
• Koch, Walter J.
• Tükel, Çagla
• Monestier, Marc
• Gamero, Ana

• Immunology
• Autoimmunity
• Curli
• Dendritic cells
• Plasmacytoid dendritic cells
• STAT2
• Systemic lupus erythematosus

Statement dc:rights

• IN COPYRIGHT- This Rights Statement can be used for an Item that is in copyright. Using this statement implies that the organization making this Item available has determined that the Item is in copyright and either is the rights-holder, has obtained permission from the rights-holder(s) to make their Work(s) available, or makes the Item available under an exception or limitation to copyright (including Fair Use) that entitles it to make the Item available.

Licence dc:rights.uri

• http://rightsstatements.org/vocab/InC/1.0/

Language dc:language.iso

eng

Handle dc:identifier.uri

http://hdl.handle.net/20.500.12613/3433

OAI identifier oai:identifier

oai:scholarshare.temple.edu:20.500.12613/3433