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Rheumatoid arthritis susceptibility genes: An overview
Author(s) -
Izabela Korczowska
Publication year - 2014
Publication title -
world journal of orthopedics
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 0.76
H-Index - 43
ISSN - 2218-5836
DOI - 10.5312/wjo.v5.i4.544
Subject(s) - rheumatoid arthritis , medicine , pathogenesis , immunology , arthritis , tumor necrosis factor alpha , gene , disease , human leukocyte antigen , autoimmune disease , bioinformatics , antigen , genetics , antibody , biology
Rheumatoid arthritis (RA) is a chronic, inflammatory autoimmune disease sustained by genetic factors. Various aspects of the genetic contribution to the pathogenetics and outcome of RA are still unknown. Several genes have been indicated so far in the pathogenesis of RA. Apart from human leukocyte antigen, large genome wide association studies have identified many loci involved in RA pathogenesis. These genes include protein tyrosine phosphatase, nonreceptor type 22, Peptidyl Arginine Deiminase type IV, signal transducer and activator of transcription 4, cytotoxic T-lymphocyte-associated protein 4, tumor necrosis factor-receptor associated factor 1/complement component 5, tumor necrosis factor and others. It is important to determine whether a combination of RA risk alleles are able to identify patients who will develop certain clinical outcomes, such myocardium infarction, severe infection or lymphoma, as well as to identify patients who will respond to biological medication therapy.

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