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Glucocorticoid-induced leucine zipper (GILZ) inhibits B cell activation in systemic lupus erythematosus.

Author(s): Amanda Light, Andrew E J Toh, Sarah Jones, Qiang Cheng, Dragana Odobasic, Simona Infantino, David Tarlinton, Eric Morand, Brendan Russ, Stefan White, Jacinta Lee, Marie-Anne Virginie Oudin, James Harris

Publication date: 2016-04-01

Journal: Annals of the Rheumatic Diseases

Publisher: BMJ

Keywords: Systemic Lupus Erythematosus, Autoantibodies, Inflammation, B cells, Autoimmunity

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Abstract

Systemic lupus erythematosus (SLE) is a serious multisystem autoimmune disease, mediated by disrupted B cell quiescence and typically treated with glucocorticoids. We studied whether B cells in SLE are regulated by the glucocorticoid-induced leucine zipper (GILZ) protein, an endogenous mediator of anti-inflammatory effects of glucocorticoids.

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PubMed ID:: 26612340

DOI:: 10.1136/annrheumdis-2015-207744

Keywords: Systemic Lupus Erythematosus,Autoantibodies,Inflammation,B cells,Autoimmunity

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Keywords: Systemic Lupus Erythematosus, Autoantibodies, Inflammation, B cells, Autoimmunity

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