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In vitro modulation of the multiple sclerosis (MS)-associated retrovirus by cytokines: implications for MS

Caterina Serra1, Giuseppe Mameli, Giannina Arru

  • 1Section of Microbiology, Department of Biomedical Sciences, University of Sassari, Sassari, Italy.

Journal of Neurovirology
|November 7, 2003
PubMed

Insights

Multiple sclerosis (MS)-associated retrovirus (MSRV) is modulated by cytokines. Pro-inflammatory cytokines increase MSRV release, while interferon beta (IFN-β) inhibits it, suggesting a therapeutic target for MS.

Area of Science:

  • Immunology
  • Neurovirology
  • Retroviruses

Background:

  • Multiple sclerosis (MS) is a chronic neurological disease.
  • The human endogenous retrovirus (HERV)-W family includes MS-associated retrovirus (MSRV).
  • MSRV exhibits gliotoxic and superantigenic properties and is linked to MS progression.

Purpose of the Study:

  • To investigate the modulation of MSRV by cytokines relevant to MS.
  • To analyze MSRV production in peripheral blood mononuclear cells (PBMCs) from MS patients.

Main Methods:

  • Utilized PBMCs from MSRV-positive and MSRV-negative individuals.
  • Cultured cells were exposed to various cytokines, including IL-4, IL-6, IFN-γ, TNF-α, and IFN-β.
  • MSRV release was quantified in response to cytokine stimulation.

Main Results:

  • MSRV was spontaneously released by cells from MSRV-positive donors but not MSRV-negative donors.
  • Interleukin-4 (IL-4) and Interleukin-6 (IL-6) increased MSRV release.
  • Interferon gamma (IFN-γ) and Tumor Necrosis Factor alpha (TNF-α) significantly enhanced MSRV production, while Interferon beta (IFN-β) inhibited it.

Conclusions:

  • Cytokine profiles observed in vitro correlate with in vivo MS disease activity.
  • IFN-β, an MS therapeutic, demonstrates inhibitory effects on MSRV release.
  • These findings suggest a potential role for MSRV and its modulation in MS pathogenesis.

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