scholarly journals The Autoimmune Tautology: From Polyautoimmunity and Familial Autoimmunity to the Autoimmune Genes

2012 ◽  
Vol 2012 ◽  
pp. 1-2 ◽  
Author(s):  
Juan-Manuel Anaya ◽  
Adriana Rojas-Villarraga ◽  
Mario García-Carrasco
Keyword(s):  
Autoimmune Tautology

scholarly journals The autoimmune tautology

2010 ◽  
Vol 12 (6) ◽  
Author(s):  
Juan-Manuel Anaya
Keyword(s):  
Autoimmune Tautology

The Multiple Autoimmune Syndromes. A Clue for the Autoimmune Tautology

2012 ◽  
Vol 43 (3) ◽  
pp. 256-264 ◽  
Author(s):  
Juan-Manuel Anaya ◽  
John Castiblanco ◽  
Adriana Rojas-Villarraga ◽  
Ricardo Pineda-Tamayo ◽  
Roger A. Levy ◽  
...  
Keyword(s):  
Autoimmune Tautology

scholarly journals A DNA-Methylated Sight on Autoimmune Inflammation Network across RA, pSS, and SLE

2018 ◽  
Vol 2018 ◽  
pp. 1-13 ◽  
Author(s):  
Xingqiang Wang ◽  
Dongyun Lei ◽  
Jie Ding ◽  
Shuang Liu ◽  
Li Tao ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Lupus Erythematosus ◽  
Inflammatory Process ◽  
Methylation Status ◽  
Differential Methylation ◽  
Promoter Regions ◽  
Bioinformatics Analyses ◽  
Epigenetic Biomarkers ◽  
The Difference ◽  
Autoimmune Tautology

Methylation variabilities of inflammatory cytokines play important roles in the development of systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and primary Sjögren’s syndrome (pSS). With heightened focus on personalized and precise medicine, it is necessary to compare and contrast the difference and similarity of cytokine methylation status between the 3 most classic autoimmune diseases (AIDs). In this study, we integrated 5 Cytokine-Chips from genome-wide DNA methylation datasets of the 3 kind of AIDs, delta-beta value was calculated for intergroup difference, and comprehensive bioinformatics analyses of cytokine genes with aberrant methylations were performed. 125 shared differential methylation variabilities (DMVs) were identified. There were 102 shared DMVs with similar methylation status; 3 hypomethylated differential methylation regions (DMRs) across the AIDs were found, and all 3 DMRs were hypomethylated. DMRs (AZU1, LTBR, and RTEL1) were likely to serve as activator in the inflammatory process. Particularly, AZU1 and LTBR with hypomethylated TSS and first exon located in the promoter regions were able to trigger inflammation signaling cascades and play critical roles in autoimmune tautology. Moreover, functional epigenetic module (FEM) algorithm showed that different inflammatory networks are involved in different AIDs; 5 hotspots were identified as biologically plausible pathways in inducing or perpetuating of inflammation which are epigenetically deregulated in AIDs. We concluded methylation variabilities among the same cytokines can greatly impact the perpetuation of inflammatory process or signal pathway of AIDs. Differentiating the cytokine methylation status will serve as valuable resource for researchers alike to gain better understanding of the epigenetic mechanisms of the three AIDs. Even more importantly, better understanding of cytokine methylation variability existing between the three classic AIDs will aid in identification of potential epigenetic biomarkers and therapeutic targets. This trial is registered with ChiCTR-INR-16010290, a clinical trial for the treatment of rheumatoid arthritis with Warming yang and Smoothening Meridians.

The autoimmune tautology. A summary of evidence

2017 ◽  
Vol 84 (3) ◽  
pp. 251-253 ◽  
Author(s):  
Juan-Manuel Anaya
Keyword(s):  
Autoimmune Tautology

scholarly journals The Autoimmune Tautology: An In Silico Approach

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Ricardo A. Cifuentes ◽  
Daniel Restrepo-Montoya ◽  
Juan-Manuel Anaya
Keyword(s):  
Protein Interactions ◽  
Lupus Erythematosus ◽  
Autoimmune Thyroid Disease ◽  
Protein Protein Interactions ◽  
Autoimmune Thyroid ◽  
Type1 Diabetes ◽  
The Common ◽  
Similarities And Differences ◽  
Autoimmune Tautology

There is genetic evidence of similarities and differences among autoimmune diseases (AIDs) that warrants looking at a general panorama of what has been published. Thus, our aim was to determine the main shared genes and to what extent they contribute to building clusters of AIDs. We combined a text-mining approach to build clusters of genetic concept profiles (GCPs) from the literature in MedLine with knowledge of protein-protein interactions to confirm if genes in GCP encode proteins that truly interact. We found three clusters in which the genes with the highest contribution encoded proteins that showed strong and specific interactions. After projecting the AIDs on a plane, two clusters could be discerned: Sjögren’s syndrome—systemic lupus erythematosus, and autoimmune thyroid disease—type1 diabetes—rheumatoid arthritis. Our results support the common origin of AIDs and the role of genes involved in apoptosis such asCTLA4,FASLG,andIL10.

The autoimmune tautology with a focus on antiphospholipid syndrome

Lupus ◽  
2014 ◽  
Vol 23 (12) ◽  
pp. 1273-1275 ◽  
Author(s):  
J-S Franco ◽  
J-M Anaya
Keyword(s):  
Antiphospholipid Syndrome ◽  
Autoimmune Tautology
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