Unopposed Immune Stimulation in Giant Cell Arteritis (GCA): A Consequence of a Reprogrammed STAT1 Signaling Pathway

Update Item Information
Identifier 20130211_nanos_sciplatform1_01-1
Title Unopposed Immune Stimulation in Giant Cell Arteritis (GCA): A Consequence of a Reprogrammed STAT1 Signaling Pathway
Creator Shalini V. Mohan; Y. J. Liao; Bryan Yang; Bjorn Hartmann; Jorg J. Goronzy; Cornelia M. Weyand
Affiliation (SVM) (BY) (BH) (JJG) (CMW) Stanford University/School of Medicine, Stanford, CA; (YJL) Stanford University/Ophthalmology, Stanford, CA
Subject Giant Cell Arteritis; Ischemic Optic Neuropathy; STAT1; CD4+ T cells; Regulatory T cells
Description GCA can manifest with severe vision loss from involvement of the ophthalmic artery or its branches. Arteritis is caused by unopposed activation of CD4+ T cells and persistent cytokine production (e.g. IL-6). In healthy immune responses, early innate cytokines (e.g. IFN-) drive feed-forward amplification loops but also promote anti-inflammatory T-regulatory cells (Treg) to contract and terminate immune reactions. We have studied whether such critical immune regulatory pathways are maintained in GCA.
Date 2013-02-11
Language eng
Format application/pdf
Format Creation Microsoft PowerPoint
Type Text
Source 2013 North American Neuro-Ophthalmology Society Annual Meeting
Relation is Part of NANOS 2013: Platform Presentations (Session I)
Collection Neuro-Ophthalmology Virtual Education Library: NANOS Annual Meeting Collection: https://novel.utah.edu/collection/nanos-annual-meeting-collection/
Publisher North American Neuro-Ophthalmology Society
Holding Institution Spencer S. Eccles Health Sciences Library, University of Utah
Rights Management Copyright 2013. For further information regarding the rights to this collection, please visit: https://NOVEL.utah.edu/about/copyright
ARK ark:/87278/s6vq68bk
Setname ehsl_novel_nam
ID 183366
Reference URL https://collections.lib.utah.edu/ark:/87278/s6vq68bk