Abstract
Systemic lupus erythematosus (SLE) is a systemic autoimmune inflammatory disease with partially understood etiology, which can affect virtually any organ. Despite suggestions to the contrary, SLE is proving to be a reliable phenotype for genetic studies. Similar to many other autoimmune diseases, SLE demonstrates a complex pattern of inheritance that is consistent with the involvement of multiple susceptibility genes as well as environmental risk factors. During the past several years, some new candidate genes have been implicated in induction of SLE through association studies, and multiple susceptibility regions have been detected through genome-wide linkage studies. Many of the susceptibility effects have been confirmed by independent studies.
Publication types
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Research Support, U.S. Gov't, Non-P.H.S.
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Research Support, U.S. Gov't, P.H.S.
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Review
MeSH terms
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Antigens, CD
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Antigens, Differentiation / genetics
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Antigens, Surface / genetics
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Apoptosis Regulatory Proteins
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CTLA-4 Antigen
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Complement System Proteins / genetics
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Genetic Linkage
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Humans
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Lupus Erythematosus, Systemic / genetics*
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Lupus Erythematosus, Systemic / immunology
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Major Histocompatibility Complex / genetics
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Mannose-Binding Lectin / genetics
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Pedigree
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Programmed Cell Death 1 Receptor
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Receptors, IgG / genetics
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Receptors, IgG / immunology
Substances
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Antigens, CD
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Antigens, Differentiation
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Antigens, Surface
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Apoptosis Regulatory Proteins
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CTLA-4 Antigen
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CTLA4 protein, human
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Mannose-Binding Lectin
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PDCD1 protein, human
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Programmed Cell Death 1 Receptor
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Receptors, IgG
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Complement System Proteins