Systemic Lupus Erythematosus: Recent Concepts in Genomics, Pathogenetic Mechanisms, and Therapies

Abstract

Systemic lupus erythematosus (SLE) is a chronic multisystem autoimmune disorder associated with multiple immunological abnormalities and a wide range of clinical manifestations. Recent progress in genetics has expanded the number of the genes associated with SLE to more than 20 in number and has contributed to improvement of understanding of the pathogenesis of the disease. This has enhanced the development of novel therapeutic targets and biomarkers for individualized and tailor-made clinical management of lupus patients. Despite this knowledge, however, it is a challenge to fully understand the genetic pathogenesis of the disease. The present paper describes the current concepts in the mechanisms, genomics, and pathogenesis of SLE and their implications for management of the disorder. The potential role of gene therapy, biological agents, intravenous immunoglobulin, anti-inflammatory cytokines, and cytokine inhibitors is discussed.

Treatment of low doses curcumin could modulate Th17/Treg balance specifically on CD4+ T cell cultures of systemic lupus erythematosus patients

“…Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with multiple organ manifestations [ 1 ]. Recently, there is a new paradigm in SLE pathogenesis involving enhancement of Th17 with a parallel reduction of Treg population in SLE patients [ 2 – 5 ].…”

Macrophage migration inhibitory factor: Association of −794 CATT5–8 and −173 G>C polymorphisms with TNF-α in systemic lupus erythematosus

“…SLE is characterized by a significant humoral response with altered proinflammatory cytokine production, suggesting a critical role for cytokines in its pathogenesis [5,7–11]. The cytokine macrophage migration inhibitory factor (MIF) is distinguished functionally by its ability to counter-regulate glucocorticoid immunosuppression and sustain pro-inflammatory activation by inhibiting activation-induced apoptosis [12].…”

Peran Imunitas Humoral Pada Penyakit Systemic Lupus Erythematosus (Sle)

“…Baik anti-dsDNA dan anti-ssDNA terlibat dalam perkembangan penyakit. Lupus seperti autoimunitas lain terjadi karena hiperaktifitas dari sel B dengan minimal atau tanpa kontribusi dari sel limfosit T. 8 Gambaran sentral dari SLE adalah kecenderungan untuk menghasilkan autoantibodi IgG dengan aviditas tinggi terhadap DNA yang mempunyai potensi patogenik. Tentu saja, banyak dari gen Ig yang mengkodekan autoantibodi terhadap DNA sudah bermutasi berat.…”