Abstract
Lupus glomerulonephritis (LN) is a complex autoimmune disease characterized by circulating autoantibodies, immune-complex deposition, immune dysregulation and defects in regulatory T cell (Tregs). Treatment options rely on general immunosuppressants and steroids that have serious side effects. Approaches to target immune cells, such as B cells in particular, has had limited success and new approaches are being investigated. Defects in Tregs in the setting of autoimmunity is well known and Treg-replacement strategies are currently being explored. The aim of this minireview is to rekindle interest on Treg-targeting strategies. We discuss the existing evidences for Treg-enhancement strategies using key cytokines interleukin (IL)-2, IL-33 and IL-6 that have shown to provide remission in LN. We also discuss strategies for indirect Treg-modulation for protection from LN.
Highlights
Systemic Lupus Erythematosus (SLE) is a debilitating autoimmune disease characterized by inflammation, increased circulating autoantibodies, immune complex (IC) deposition, and multi-organ dysfunction affecting skin, joints, kidneys, brain etc
IL-2 deficiency may contribute to autoimmunity in SLE patients and lupus-prone mice by inducing paucity of Tregs, defective activation-induced cell death (AICD) and increased IL-17 production (Lippe et al, 2012)
An interesting study focusing on the safety and efficacy of low dose IL-2 in 11 autoimmune disease in 46 patients including SLE found significant Treg-expansion without effector T-cell activation (Rosenzwajg et al, 2019)
Summary
Reviewed by: Niklas Beyersdorf, Julius Maximilian University of Würzburg, Germany. Lupus glomerulonephritis (LN) is a complex autoimmune disease characterized by circulating autoantibodies, immune-complex deposition, immune dysregulation and defects in regulatory T cell (Tregs). Approaches to target immune cells, such as B cells in particular, has had limited success and new approaches are being investigated. Defects in Tregs in the setting of autoimmunity is well known and Treg-replacement strategies are currently being explored. The aim of this minireview is to rekindle interest on Treg-targeting strategies. We discuss the existing evidences for Tregenhancement strategies using key cytokines interleukin (IL)-2, IL-33 and IL-6 that have shown to provide remission in LN. We discuss strategies for indirect Treg-modulation for protection from LN
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