狼疮性肾炎
免疫学
免疫系统
发病机制
医学
系统性红斑狼疮
肾炎
肾
病理
疾病
内科学
作者
Rhea Bhargava,Hao Li,George C. Tsokos
出处
期刊:Current Opinion in Rheumatology
[Ovid Technologies (Wolters Kluwer)]
日期:2022-07-05
卷期号:35 (2): 107-116
被引量:19
标识
DOI:10.1097/bor.0000000000000887
摘要
Purpose of review Lupus nephritis is associated with significant mortality and morbidity. We lack effective therapeutics and biomarkers mostly because of our limited understanding of its complex pathogenesis. We aim to present an overview of the recent advances in the field to gain a deeper understanding of the underlying cellular and molecular mechanisms involved in lupus nephritis pathogenesis. Recent findings Recent studies have identified distinct roles for each resident kidney cell in the pathogenesis of lupus nephritis. Podocytes share many elements of innate and adaptive immune cells and they can present antigens and participate in the formation of crescents in coordination with parietal epithelial cells. Mesangial cells produce pro-inflammatory cytokines and secrete extracellular matrix contributing to glomerular fibrosis. Tubular epithelial cells modulate the milieu of the interstitium to promote T cell infiltration and formation of tertiary lymphoid organs. Modulation of specific genes in kidney resident cells can ward off the effectors of the autoimmune response including autoantibodies, cytokines and immune cells. Summary The development of lupus nephritis is multifactorial involving genetic susceptibility, environmental triggers and systemic inflammation. However, the role of resident kidney cells in the development of lupus nephritis is becoming more defined and distinct. More recent studies point to the restoration of kidney resident cell function using cell targeted approaches to prevent and treat lupus nephritis.
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