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Gac Med Mex. 2014 Jul-Aug;150(4):334-44.

[Tumor necrosis factor alpha (TNF-α) in autoimmune diseases (AIDs): molecular biology and genetics].

[Article in Spanish]

Author information

1
Departamento de Biología Molecular, Instituto Nacional de Cardiología, México, D.F.
2
Departamento de Biología Molecular, Instituto Nacional de Cardiología, México, D.F.; Subdirección de Investigación Básica y Tecnológica, Instituto Nacional de Cardiología, México, D.F.
3
Laboratorio de Inmunogenómica y Enfermedades Metabólicas, Instituto Nacional de Medicina Genómica, México, D.F.
4
Laboratorio de Genética y Diagnóstico Molecular, Unidad de Investigación, Hospital Juárez de México, México, D.F.
5
Laboratorio de Medicina Genómica, Unidad de Investigación, Hospital Juárez de México, México, D.F.

Abstract

It has been estimated that autoimmune diseases (AIDs) affect 5-8% of the US population. AIDs are a serious public health problem worldwide. These diseases are chronic conditions initiated by the loss of immunological tolerance to self-antigens. AIDs cause various clinical consequences ranging from mild to severe, affecting one or more target organs and repeatedly causing the patient's death. Five of the most common AIDs are rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), Graves´ disease (GD), insulin-dependent diabetes mellitus or type I (T1DM), and multiple sclerosis (MS). The TNF-α gene and its protein product, the cytokine TNF-α, play an important role in the pathogenesis of EAs. The anti-TNF-α therapies using monoclonal antibodies directed against TNF-α have shown good results in diseases such as RA, JRA, but not in other EA such as SLE and MS. This review focuses on presenting to the reader the biological role of TNF-α under normal conditions and the initiation, development, susceptibility, severity, and treatment response of the most common AIDs.

PMID:
25098219
[Indexed for MEDLINE]
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