alexa Disease-Specific and Common HLA and Non-HLA Genetic Markers in Susceptibility to Rheumatoid Arthritis, Type 1 Diabetes Mellitus and Multiple Sclerosis
ISSN: 1747-0862

Journal of Molecular and Genetic Medicine
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Review Article

Disease-Specific and Common HLA and Non-HLA Genetic Markers in Susceptibility to Rheumatoid Arthritis, Type 1 Diabetes Mellitus and Multiple Sclerosis

Tatjana Sjakste1, Jolanta Kalnina1, Natalia Paramonova1, Liene Nikitina-Zake2 and Nikolajs Sjakste3,4*

1Genomics and Bioinformatics, Institute of Biology of the University of Latvia, Salaspils, Latvia

2Latvian Biomedical Research and Study Centre, Riga LV1067, Latvia

3Department of Medical Biochemistry, Faculty of Medicine, University of Latvia, Riga LV-1004, Latvia

4Latvian Institute of Organic Synthesis, Riga LV-1006, Latvia

Corresponding Author:
Nikolajs Sjakste
Latvian Institute of Organic Synthesis
No. 21 Aizkraukles Street, Riga LV-1006, Latvia
Tel: 371-29198804
Fax: 371-67034369
E-mail: [email protected]

Received date: February 28, 2014 Accepted date: April 11, 2014 Published date: April 21, 2014

Citation: Sjakste T, Kalnina J, Paramonova N, Nikitina-Zake L, Sjakste N (2014) Disease-Specific and Common HLA and Non-HLA Genetic Markers in Susceptibility to Rheumatoid Arthritis, Type 1 Diabetes Mellitus and Multiple Sclerosis. J Mol Genet Med 8:119. doi: 10.4172/1747-0862.1000119

Copyright: © 2014 Sjakste T, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Autoimmune diseases cause numerous health and social problems throughout the world. The common spectrum of autoimmune diseases affect the majority of tissues within the body, including pancreatic beta cells in type 1 diabetes (T1DM), myelin surrounding nerve axons in Multiple sclerosis (MS) and synovial joint antigens in Rheumatoid Arthritis (RA). The diseases are likely caused by a complex interaction between multiple HLA- and non- HLA related genes and environmental factors. The well documented co-clustering of autoimmune diseases within families and individuals, together with apparent sharing of number risk genes between the diseases suggests at least some common mechanisms of autoimmune development.

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