Restoring regulation - IL-2 therapy in systemic lupus erythematosus

被引:39
|
作者
Humrich, Jens Y. [1 ]
Riemekasten, Gabriela [1 ]
机构
[1] Univ Hosp Schleswig Holstein, Dept Rheumatol, Campus Lubeck,Ratzeburger Allee 160, D-23538 Lubeck, Germany
关键词
SLE; regulatory T cell; interleukin-2; immunotherapy; tolerance; immune homeostasis; systemic lupus erythematosus; LOW-DOSE INTERLEUKIN-2; RESPONSIVE ELEMENT MODULATOR; T-CELLS; AUTOIMMUNE-DISEASE; SELF-TOLERANCE; VIVO EXPANSION; PRONE MICE; EX-VIVO; FOXP3; EXPRESSION;
D O I
10.1080/1744666X.2016.1199957
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Introduction: The pathogenesis of systemic lupus erythematosus (SLE) involves an acquired deficiency of the cytokine IL-2, an essential growth and survival factor for regulatory T cells (Treg), which play an important role in the control of autoimmunity in SLE. In contrast to currently available therapies that broadly suppress the immune system, low-dose IL-2 therapy in SLE aims to compensate the pre-existing IL-2 deficiency and thus to restore a physiological state, where Treg can regain their ability to efficiently counteract autoimmunity.Areas covered: Here we summarize key findings that led to the development of this novel therapeutic concept and will highlight the key rationales for the clinical translation of low-dose IL-2 therapy in SLE.Expert commentary: The concept of low-dose IL-2 therapy in SLE has evolved from pathophysiological findings and thus can be considered a selective biological treatment strategy in SLE. Preliminary results from phase I/II studies are promising by proving selective Treg expansion and by providing first evidence for the clinical efficacy of low-dose IL-2 therapy in SLE.
引用
收藏
页码:1153 / 1160
页数:8
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