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TNFAIP3 regulates inflammatory arthritis through the differentiation of monocytes into macrophages

Lu Zhang1, Wanlan Jiang1, Biqing Zhang1

  • 1Department of Rheumatology and Immunology, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu Province, People's Republic of China.

Asian Pacific Journal of Allergy and Immunology
|June 3, 2025
PubMed
Abstract

Insights

Tumor necrosis factor-α inducible protein 3 (TNFAIP3) in monocytes helps regulate rheumatoid arthritis by controlling cell migration and differentiation. Upregulating TNFAIP3 reduces inflammation and arthritis severity.

Area of Science:

  • Immunology
  • Molecular Biology
  • Rheumatology

Background:

  • Rheumatoid arthritis (RA) is an inflammatory disease characterized by synovitis, with RA synovium rich in macrophages derived from monocytes.
  • Tumor necrosis factor-α inducible protein 3 (TNFAIP3) is an RA susceptibility gene with known anti-inflammatory properties.
  • Previous research indicated abnormal TNFAIP3 protein expression in monocytes from RA patients.

Purpose of the Study:

  • To investigate the role of TNFAIP3 within monocytes in the context of rheumatoid arthritis.
  • To explore the functional significance of TNFAIP3 in monocyte behavior relevant to RA pathogenesis.

Main Methods:

  • In vivo: Adenoviral vectors overexpressing tnfaip3 were administered to mice with collagen-induced arthritis (CIA).
  • In vitro: Lentivirus transfection was used to modulate tnfaip3 expression in THP-1 cells.
  • Evaluated monocyte migration, cytokine secretion, macrophage differentiation, and arthritis scores.

Main Results:

  • Overexpression of TNFAIP3 in mice ameliorated arthritis, reduced pro-inflammatory iNOS+ cells, and increased anti-inflammatory CD206+ cells in the synovium.
  • In vitro, TNFAIP3 depletion enhanced monocyte migration and M1 macrophage differentiation, while TNFAIP3 overexpression promoted M2 macrophage differentiation.
  • TNFAIP3-depleted cells exhibited increased secretion of pro-inflammatory cytokines IL-6 and MMPs.

Conclusions:

  • TNFAIP3 plays a crucial role in regulating inflammatory arthritis.
  • TNFAIP3 modulates monocyte migration, differentiation into M1/M2 macrophages, and cytokine secretion.
  • Targeting TNFAIP3 in monocytes presents a potential therapeutic strategy for rheumatoid arthritis.

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