z-logo
open-access-imgOpen Access
The genetic basis of systemic lupus erythematosus--knowledge of today and thoughts for tomorrow
Author(s) -
Ludmila ProkuninaOlsson
Publication year - 2004
Publication title -
human molecular genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.811
H-Index - 276
eISSN - 1460-2083
pISSN - 0964-6906
DOI - 10.1093/hmg/ddh076
Subject(s) - autoimmune disease , immunology , disease , biology , genetic predisposition , lupus erythematosus , allele , etiology , systemic lupus erythematosus , autoimmunity , systemic disease , genetics , immunopathology , medicine , immune system , gene , antibody , pathology
Systemic lupus erythematosus (SLE) is a chronic rheumatic disease with an autoimmune etiology. Nuclear components of the cells are the main targets of the autoimmune reaction, affecting virtually any organ in the body. SLE is also called a prototype disease due to a substantial overlap in its clinical symptoms with other autoimmune diseases. Therefore the understanding of the mechanisms underlying SLE may contribute to advances in studies and development of new treatments for several autoimmune diseases. SLE is a complex disease with both genetic factors (mutations or susceptibility alleles) and environmental factors (infections, drugs, stress, exposures, etc.) contributing to its development. In this article we will give an overview of the latest findings in genetics of SLE, concentrating on the two most interesting and promising pathways: the PD-1 and the interferon pathways.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.
Having issues? You can contact us here
Accelerating Research

Address

John Eccles House
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom