Upregulation of the C/EBP β LAP isoform could be due to decreased TNFAIP3/TNIP1 expression in the peripheral blood mononuclear cells of patients with systemic lupus erythematosus

Abstract

Objectives: We aimed to examine CCAAT/enhancer-binding protein β (C/EBP β), TNF-alpha-induced protein 3 (TNFAIP3), and TNFAIP3-interacting protein 1 (TNIP1) expression in peripheral blood mononuclear cells (PBMCs) of systemic lupus erythematosus (SLE) patients to assess their relationship in SLE pathogenesis.

Methods: C/EBP β, TNIP1, and TNFAIP3 expression was assessed in PBMCs from 20 SLE patients and 20 controls by western blotting. The correlation between C/EBP β/TNFAIP3/TNIP1 expression and SLE disease activity was determined by Spearman’s rank. C/EBP β, TNIP1, and TNFAIP3 levels in THP-1 cells, THP-1 cells transfected with plasmids encoding TNFAIP3 shRNA, and THP-1 cells infected with lentiviral vectors encoding TNIP1 shRNA were assessed by western blotting.

Results: C/EBP β LAP isoform expression was increased and LIP/TNFAIP3/TNIP1 expression was decreased in SLE patients. LAP expression was positively correlated with SLE disease activity; TNFAIP3 and TNIP1 expression was negatively correlated with SLE disease activity. LAP expression was increased in SLE patients with proteinuria and elevated anti-dsDNA antibody, as well as in THP-1 cells transfected with plasmids encoding TNFAIP3 shRNA and THP-1 cells infected with lentiviral vectors encoding TNIP1 shRNA.

Conclusions: C/EBP β/TNFAIP3/TNIP1 is associated with SLE activity. The upregulated expression of C/EBP β LAP could be caused by reduced TNFAIP3/TNIP1 expression.

Keywords:

• Autoimmunity
• CCAAT/enhancer-binding protein β
• SLE
• TNF-alpha-induced protein 3
• TNFAIP3-interacting protein 1

Acknowledgments

We wish to thank Professor Bing Ni (Institute of Immunology, PLA, Third Military Medical University, China) for suggestions regarding experimental methods and research ideas.

Conflict of interest

The authors declare that no conflicts of interest exist.

This work was supported by grants from the National Natural Science Foundation of China [Nos. 81201232 and 81472883].