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Semaphorin 3G exacerbates joint inflammation through the accumulation and proliferation of macrophages in the

Jumpei Shoda1,2, Shigeru Tanaka1, Keishi Etori1

  • 1Department of Allergy and Clinical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.

Arthritis Research & Therapy
|June 6, 2022
PubMed
Abstract

Insights

Methotrexate (MTX) treatment downregulates semaphorin 3G in rheumatoid arthritis (RA) patients. This protein exacerbates joint inflammation by increasing macrophage accumulation, suggesting a new therapeutic target for RA.

Area of Science:

  • Immunology
  • Rheumatology
  • Molecular Biology

Background:

  • Methotrexate (MTX) is a primary treatment for rheumatoid arthritis (RA), but its exact mechanisms of action are not fully understood.
  • Identifying novel therapeutic targets is crucial for improving RA treatment outcomes.

Purpose of the Study:

  • To identify novel therapeutic target molecules affected by MTX in RA patients.
  • To investigate the role of semaphorin 3G and its receptor neuropilin-2 in RA pathogenesis.

Main Methods:

  • DNA microarray analysis of CD4+ T cells from RA patients before and after MTX treatment.
  • Evaluation of semaphorin 3G and neuropilin-2 expression in RA and osteoarthritis synovium.
  • Studies in semaphorin3G-deficient mice and in vitro analysis of macrophage behavior.

Main Results:

  • MTX treatment downregulated semaphorin 3G expression in RA patient CD4+ T cells.
  • Semaphorin 3G was upregulated in RA synovium, with its receptor neuropilin-2 on activated macrophages.
  • Semaphorin3G deficiency ameliorated arthritis models, while semaphorin 3G enhanced macrophage migration and proliferation.

Conclusions:

  • Upregulation of semaphorin 3G in the RA synovium is a novel mechanism contributing to joint inflammation.
  • Semaphorin 3G exacerbates RA by promoting macrophage accumulation, indicating its potential as a therapeutic target.
Keywords:
MacrophageMethotrexateNeuropilin-2Rheumatoid arthritisSemaphorin

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