Common mechanisms of autoimmune diseases (the autoimmune tautology)

Juan Manuel Anaya

doi:10.1016/j.autrev.2012.02.002

Common mechanisms of autoimmune diseases (the autoimmune tautology)

Juan Manuel Anaya

Research output: Contribution to Journal › Review article › peer-review

111 Scopus citations

Abstract

The fact that autoimmune diseases share subphenotypes, physiopathological mechanisms and genetic factors has been called autoimmune tautology, and indicates that they have a common origin. The autoimmune phenotypes vary depending on the target cell and the affected organ, gender, ancestry, trigger factors and age at onset. Ten shared characteristics supporting this logical theory are herein reviewed.

Original language	English (US)
Pages (from-to)	781-784
Number of pages	4
Journal	Autoimmunity Reviews
Volume	11
Issue number	11
DOIs	https://doi.org/10.1016/j.autrev.2012.02.002
State	Published - Sep 2012

All Science Journal Classification (ASJC) codes

Immunology and Allergy
Immunology

Access to Document

10.1016/j.autrev.2012.02.002

Cite this

@article{ec4cc8624ca24f4782ea041d6d754efc,

title = "Common mechanisms of autoimmune diseases (the autoimmune tautology)",

abstract = "The fact that autoimmune diseases share subphenotypes, physiopathological mechanisms and genetic factors has been called autoimmune tautology, and indicates that they have a common origin. The autoimmune phenotypes vary depending on the target cell and the affected organ, gender, ancestry, trigger factors and age at onset. Ten shared characteristics supporting this logical theory are herein reviewed.",

author = "Anaya, \{Juan Manuel\}",

note = "Funding Information: All the members of the Center of Autoimmune Diseases Research (CREA) are so thankful for their contributions and fruitful discussions. This work is supported by the School of Medicine and Health Sciences of Universidad del Rosario , and Colciencias , Bogota, Colombia. Copyright: Copyright 2013 Elsevier B.V., All rights reserved.",

year = "2012",

month = sep,

doi = "10.1016/j.autrev.2012.02.002",

language = "English (US)",

volume = "11",

pages = "781--784",

journal = "Autoimmunity Reviews",

issn = "1568-9972",

publisher = "Elsevier BV",

number = "11",

}

TY - JOUR

T1 - Common mechanisms of autoimmune diseases (the autoimmune tautology)

AU - Anaya, Juan Manuel

N1 - Funding Information: All the members of the Center of Autoimmune Diseases Research (CREA) are so thankful for their contributions and fruitful discussions. This work is supported by the School of Medicine and Health Sciences of Universidad del Rosario , and Colciencias , Bogota, Colombia. Copyright: Copyright 2013 Elsevier B.V., All rights reserved.

PY - 2012/9

Y1 - 2012/9

N2 - The fact that autoimmune diseases share subphenotypes, physiopathological mechanisms and genetic factors has been called autoimmune tautology, and indicates that they have a common origin. The autoimmune phenotypes vary depending on the target cell and the affected organ, gender, ancestry, trigger factors and age at onset. Ten shared characteristics supporting this logical theory are herein reviewed.

AB - The fact that autoimmune diseases share subphenotypes, physiopathological mechanisms and genetic factors has been called autoimmune tautology, and indicates that they have a common origin. The autoimmune phenotypes vary depending on the target cell and the affected organ, gender, ancestry, trigger factors and age at onset. Ten shared characteristics supporting this logical theory are herein reviewed.

UR - https://www.scopus.com/pages/publications/84862136377

UR - https://www.scopus.com/pages/publications/84862136377#tab=citedBy

U2 - 10.1016/j.autrev.2012.02.002

DO - 10.1016/j.autrev.2012.02.002

M3 - Review article

C2 - 22353402

AN - SCOPUS:84862136377

SN - 1568-9972

VL - 11

SP - 781

EP - 784

JO - Autoimmunity Reviews

JF - Autoimmunity Reviews

IS - 11

ER -

Common mechanisms of autoimmune diseases (the autoimmune tautology)

Abstract

All Science Journal Classification (ASJC) codes

Access to Document

Other files and links

Fingerprint

Cite this