Abstract
Systemic lupus erythematosus (SLE) is a devastating and heterogeneous autoimmune disease that affects multiple organs, and for which the underlying causes are unknown. The majority of SLE patients produce autoantibodies, have increased levels of type-I inflammatory cytokines, and can develop glomerulonephritis. Recent studies indicate an unexpected but strong association between increased disease activity in SLE patients and the expression of the DNA-binding protein ARID3a (A + T rich interaction domain protein 3a) in a number of peripheral blood cell types. ARID3a expression was first associated with autoantibody production in B cells; however, more recent findings also indicate associations with expression of the inflammatory cytokine interferon alpha in SLE plasmacytoid dendritic cells and low-density neutrophils. In addition, ARID3a is expressed in hematopoietic stem cells and some adult kidney progenitor cells. SLE cells expressing enhanced ARID3a levels show differential gene expression patterns compared with homologous healthy control cells, identifying new pathways potentially regulated by ARID3a. The associations of ARID3a expression with increased disease severity in SLE, suggest that it, or its downstream targets, may provide new therapeutic targets for SLE.
Highlights
The autoimmune disease systemic lupus erythematosus (SLE) affects approximately one millionAmericans [1], with symptoms ranging from rash and fatigue, to severe organ dysfunction [2,3].Disease severity varies according to the degree of organ involvement, and the level of inflammation and systemic deposition of autoantibody-containing immune complexes, and is quantified using scores that combine measurements of these criteria as SLE disease activity indices (SLEDAI scores) [2,3].The underlying mechanisms that lead to SLE are unknown, but several key features of the disease are present in the majority of patients
We found that SLE low-density neutrophils (LDNs) showed increased levels of ARID3a protein expression compared with LDNs from healthy controls (Figure 2) [49]
Gene expression data from plasmacytoid dendritic cells (pDCs) and LDNs with high levels of ARID3a protein provide new insights into genes associated with autoimmunity and increases in SLEDAI scores
Summary
The autoimmune disease systemic lupus erythematosus (SLE) affects approximately one million. The underlying mechanisms that lead to SLE are unknown, but several key features of the disease are present in the majority of patients These include breaks in humoral tolerance that result in the production of autoimmune antibodies; inflammation typically characterized by increased levels of. A number of contributing factors are likely to influence SLE pathology, in this review, we pathology, in this review, we will highlight the molecular and cellular associations of ARID3a with the will highlight the molecular and cellular associations of ARID3a with the common lupus pathologies common lupus pathologies of autoantibody production, interferon induction, and the promotion of of autoantibody production, interferon induction, and the promotion of clinical nephritis. Requires dimerization and association with both Bruton’s tyrosine kinase (BTK) and TFII-I (Transcription and TFII-I (Transcription Factor II-I) for activity in B lymphocytes [8,12,13].
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