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J Autoimmun. 2019 Jan;96:158-167. doi: 10.1016/j.jaut.2018.09.013. Epub 2018 Oct 5.

ARID3a gene profiles are strongly associated with human interferon alpha production.

Author information

1
Department of Medicine, Oklahoma City, OK, USA.
2
Department of Chemistry and Biochemistry, University of Oklahoma, Norman, OK, USA.
3
Arthritis and Clinical Immunology Program, Oklahoma City, OK, USA; Division of Genomics and Data Sciences, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA.
4
Department of Microbiology and Immunology, Oklahoma City, OK, USA.
5
Arthritis and Clinical Immunology Program, Oklahoma City, OK, USA.
6
Arthritis and Clinical Immunology Program, Oklahoma City, OK, USA; Department of Biochemistry, Oklahoma City, OK, USA.
7
Department of Medicine, Oklahoma City, OK, USA; Arthritis and Clinical Immunology Program, Oklahoma City, OK, USA; Department of Pathology, and Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.
8
Department of Medicine, Oklahoma City, OK, USA; Department of Microbiology and Immunology, Oklahoma City, OK, USA; Department of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA. Electronic address: carol-webb@ouhsc.edu.

Abstract

Type I interferons (IFN) causes inflammatory responses to pathogens, and can be elevated in autoimmune diseases such as systemic lupus erythematosus (SLE). We previously reported unexpected associations of increased numbers of B lymphocytes expressing the DNA-binding protein ARID3a with both IFN alpha (IFNα) expression and increased disease activity in SLE. Here, we determined that IFNα producing low density neutrophils (LDNs) and plasmacytoid dendritic cells (pDCs) from SLE patients exhibit strong associations between ARID3a protein expression and IFNα production. Moreover, SLE disease activity indices correlate most strongly with percentages of ARID3a+ LDNs, but were also associated, less significantly, with IFNα expression in LDNs and pDCs. Hierarchical clustering and transcriptome analyses of LDNs and pDCs revealed SLE patients with low ARID3a expression cluster with healthy controls and identified gene profiles associated with increased proportions of ARID3a- and IFNα-expressing cells of each type. These data identify ARID3a as a potential transcription regulator of IFNα-related inflammatory responses and other pathways important for SLE disease activity.

KEYWORDS:

ARID3a; Interferon alpha; Low density neutrophils; Lupus; Plasmacytoid dendritic cells

PMID:
30297159
PMCID:
PMC6497177
[Available on 2020-01-01]
DOI:
10.1016/j.jaut.2018.09.013
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