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The Autoimmune Tautology: from Polyautoimmunity and Familial Autoimmunity to the Autoimmune Genes

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The Autoimmune Tautology: from Polyautoimmunity and Familial Autoimmunity to the Autoimmune Genes Autoimmune Diseases The Autoimmune Tautology: From Polyautoimmunity and Familial Autoimmunity to the Autoimmune Genes Guest Editors: Juan-Manuel Anaya, Adriana Rojas-Villarraga, and Mario García-Carrasco The Autoimmune Tautology: From Polyautoimmunity and Familial Autoimmunity to the Autoimmune Genes Autoimmune Diseases The Autoimmune Tautology: From Polyautoimmunity and Familial Autoimmunity to the Autoimmune Genes Guest Editors: Juan-Manuel Anaya, Adriana Rojas-Villarraga, and Mario Garc´ıa-Carrasco Copyright © 2012 Hindawi Publishing Corporation. All rights reserved. This is a special issue published in “Autoimmune Diseases.” All articles are open access articles distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is prop- erly cited. Editorial Board Corrado Betterle, Italy Evelyn Hess, USA Markus Reindl, Austria Maria Bokarewa, Sweden Stephen Holdsworth, Australia P. Santamaria, Canada Nalini S. Bora, USA Hiroshi Ikegami, Japan Giovanni Savettieri, Italy D. N. Bourdette, USA Francesco Indiveri, Italy Jin-Xiong She, USA Ricard Cervera, Spain P. L. Invernizzi, Italy Animesh A. Sinha, USA Edward K. L. Chan, USA Annegret Kuhn, Germany Jan Storek, Canada M. Cutolo, Italy I. R. Mackay, Australia Alexander J. Szalai, USA George N. Dalekos, Greece Rizgar Mageed, UK Ronald Tuma, USA Thomas Dorner,¨ Germany Grant Morahan, Australia Frode Vartdal, Norway Sudhir Gupta, USA Kamal D. Moudgil, USA Edmond J. Yunis, USA Martin Herrmann, Germany Andras Perl, USA Contents The Autoimmune Tautology: From Polyautoimmunity and Familial Autoimmunity to the Autoimmune Genes, Juan-Manuel Anaya, Adriana Rojas-Villarraga, and Mario Garc´ıa-Carrasco Volume 2012, Article ID 297193, 2 pages Shared HLA Class II in Six Autoimmune Diseases in Latin America: A Meta-Analysis, Paola Cruz-Tapias, Oscar M. Perez-Fern´ andez,´ Adriana Rojas-Villarraga, Alberto Rodr´ıguez-Rodr´ıguez, Mar´ıa-Teresa Arango, and Juan-Manuel Anaya Volume 2012, Article ID 569728, 10 pages Lupus Nephritis: An Overview of Recent Findings, Alberto de Zubiria Salgado and Catalina Herrera-Diaz Volume 2012, Article ID 849684, 21 pages Epigenetics and Autoimmune Diseases, Paula Quintero-Ronderos and Gladis Montoya-Ortiz Volume 2012, Article ID 593720, 16 pages The Biological Significance of Evolution in Autoimmune Phenomena, Carlos A. Canas˜ and Felipe Canas˜ Volume 2012, Article ID 784315, 12 pages The Autoimmune Tautology: An In Silico Approach, Ricardo A. Cifuentes, Daniel Restrepo-Montoya, and Juan-Manuel Anaya Volume 2012, Article ID 792106, 10 pages Introducing Polyautoimmunity: Secondary Autoimmune Diseases No Longer Exist, Adriana Rojas-Villarraga, Jenny Amaya-Amaya, Alberto Rodriguez-Rodriguez, Ruben´ D. Mantilla, and Juan-Manuel Anaya Volume 2012, Article ID 254319, 9 pages Autoimmunity in Rheumatic Diseases Is Induced by Microbial Infections via Crossreactivity or Molecular Mimicry, Taha Rashid and Alan Ebringer Volume 2012, Article ID 539282, 9 pages Spondyloarthropathies in Autoimmune Diseases and Vice Versa, Oscar M. Perez-Fern´ andez,´ Ruben´ D. Mantilla, Paola Cruz-Tapias, Alberto Rodriguez-Rodriguez, Adriana Rojas-Villarraga, and Juan-Manuel Anaya Volume 2012, Article ID 736384, 7 pages Effect of Selenium on HLA-DR Expression of Thyrocytes, Csaba Balazs´ and Viktoria´ Kaczur Volume 2012, Article ID 374635, 5 pages Genetic Factors of Autoimmune Thyroid Diseases in Japanese, Yoshiyuki Ban Volume 2012, Article ID 236981, 9 pages How Does Age at Onset Influence the Outcome of Autoimmune Diseases?,ManuelJ.Amador-Patarroyo, Alberto Rodriguez-Rodriguez, and Gladis Montoya-Ortiz Volume 2012, Article ID 251730, 7 pages Local Cartilage Trauma as a Pathogenic Factor in Autoimmunity (One Hypothesis Based on Patients with Relapsing Polychondritis Triggered by Cartilage Trauma), Carlos A. Canas˜ and Fabio Bonilla Abad´ıa Volume 2012, Article ID 453698, 3 pages Hindawi Publishing Corporation Autoimmune Diseases Volume 2012, Article ID 297193, 2 pages doi:10.1155/2012/297193 Editorial The Autoimmune Tautology: From Polyautoimmunity and Familial Autoimmunity to the Autoimmune Genes Juan-Manuel Anaya,1 Adriana Rojas-Villarraga,1 and Mario Garcıa-Carrasco´ 2 1 Center for Autoimmune Diseases Research (CREA), School of Medicine and Health Sciences, Universidad del Rosario, Carrera 24 No. 63-C-69, Bogota, Colombia 2 Systemic Autoimmune Diseases Research Unit, Hospital General Regional No. 36, IMSS and Rheumatology Department, School of Medicine, Benem´erita Universidad Autonoma´ de Puebla, Puebla P4E, Mexico Correspondence should be addressed to Juan-Manuel Anaya, [email protected] Received 7 March 2012; Accepted 7 March 2012 Copyright © 2012 Juan-Manuel Anaya et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Autoimmune diseases (ADs) are chronic conditions initiated may differ from one AD to another one. In addition, trigger by the loss of immunological tolerance to self-antigens and factors as well as the age at onset may vary among them and represent a heterogeneous group of disorders that afflict spe- from one patient to another. Yet, autoimmune mechanisms cific target organs or multiple organ systems [1]. The chronic of injury may be common including predisposing and pro- nature of these diseases places a significant burden on the uti- tective factors. One step forward to the demonstration of this lization of medical care, direct and indirect economic costs, logically valid formula will be a new taxonomy of ADs based and quality of life. The fact that ADs share several clinical on common and specific subphenotypes that will allow us signs and symptoms (i.e., subphenotypes), physiopatho- to predict and prevent them, tailor individual medical deci- logical mechanisms, and genetic factors has been called sions, and provide personalized healthcare while facilitating autoimmune tautology and indicates that they have common patient’s participation in their treatment and eventual cure mechanisms [2–8]. of their disease. In clinical practice, there are two conditions supporting In Table 1, ten shared characteristics supporting the this theory: polyautoimmunity and familial autoimmunity. autoimmune tautology are summarized. In this special issue Polyautoimmunity is the presence of two or more ADs in of Autoimmune Diseases, adozenofpapersaredevotedto a single patient while familial autoimmunity occurs when these characteristics. Evolution and genetics of ADs, includ- different relatives from a nuclear family present with diverse ing the biological significance of evolution in autoimmune ADs [4]. These conditions indicate that similar genetic, phenomena, a meta-analysis of HLA class II in six ADs epigenetic, and environmental factors influence ADs [8]. in Latin America, genetic factors of autoimmune thyroid In rhetoric, tautology (from Greek tauto, “the same” and diseases in Japanese, and an in silico approach of the logos, “word/idea”) is an obvious statement. In medical prac- autoimmune tautology are included. An updated review on tice, Sjogren’s¨ syndrome could be considered the “autoim- epigenetics and ADs is also presented. mune diabetes” or the “celiac disease” of the salivary and Environmental factors play an important role in the lachrymal glands. In logic, tautology is a formula, which is induction of ADs. This special issue also contains a very true in every possible interpretation. Thus, autoimmune tau- interesting hypothesis about local cartilage trauma as a tology means that an AD is similar to a second one, to a third pathogenic trigger factor of autoimmunity, a review about one, and so on. Its formula is Vpq = AD1 AD2 AD3, the induction of autoimmunity by microbial infections, and where Vpq represents the symbol of tautology. ADs cannot another one on the effect of selenium on HLA-DR expression be all identical because the target cell and the affected organ of thyrocytes. How does age at onset influence the outcome 2 Autoimmune Diseases Table 1: Shared characteristics among autoimmune diseases (ADs) supporting the autoimmune tautology∗. Characteristic Comment Female predominance The more frequent the AD and the later it appears, the more women are affected. Damage induced by T or B cells, or both, plays a major pathogenic role in ADs. Although Similar pathophysiology the autoimmune phenotype varies depending on the target cell and the affected organ, the local mechanisms for tissue injury are similar. Mathematical approaches for precisely defining subphenotypes based on accurate clinical Shared subphenotypes and immunological databases, combined with strengthening molecular genetics analyses, have significant promise for a better understanding of ADs. Age at onset influences severity Early age at onset is a poor prognostic factor for some ADs. Although a latitudinal gradient of infectious agents exists, Epstein-Barr virus and cytomegalovirus are notorious as they are consistently associated with multiple ADs. Some Similar environmental factors infections could be protective against ADs development. Smoking has also been consistently associated with several ADs. Ancestry influences clinical presentation Amerindian ancestry influences the risk of acquiring ADs as well as its severity. The genetic risk factors for ADs consist of two forms: those common to many ADs and those specific to a given disorder. Combinations
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