The antiinflammatory cytokine interleukin-13 is not detectable in the circulation of multiple sclerosis patients and is not inducible by interferon-β1b treatment, that neither modifies its ex vivo secretion from peripheral blood mononuclear cells

F. Nicoletti, R. Di Marco, F. Patti, A. Nicoletti, C. Leonardi, E. Reggio, P. Meroni, A. Reggio

Research output: Contribution to journalArticlepeer-review

Abstract

Interleukin (IL)-13 is a T-cell derived cytokine closely related to IL-4 that possesses powerful antiinflammatory properties. In this study we have evaluated the blood levels of IL-13 in patients with multiple sclerosis (MS), either with relapsing remitting or secondary chronic progressive (CP) course of the disease, and have also examined the effect of treatment with interferon (IFN)-β 1b given on alternate days for 10 days both on the serum levels of IL-13 and on the ex vivo secretory capacity of mononuclear cells from MS patients. IL-13 was not detectable in the circulation of MS patients regardless of whether RR MS patients with stable or active disease or those suffering from secondary CP MS were studied. Moreover, circulating levels of IL-13 were not induced by treatment with IFN-β1b, that was neither capable of modifying the ex vivo IL-13 secretory capacity of peripheral blood mononuclear cells. These data neither anticipate a role for endogenous IL-13 in down-regulating immunoinflammation during MS attacks nor suggest that IFN-β1b treatment exerts its favourable effects on the course of RR MS by augmenting the secretion of this antiinflammatory cytokine.

Original languageEnglish
Pages (from-to)265-270
Number of pages6
JournalAutoimmunity
Volume32
Issue number4
Publication statusPublished - 2000

Keywords

  • Cytokines
  • Interferon-β
  • Interleukin-13
  • Multiple sclerosis

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Fingerprint Dive into the research topics of 'The antiinflammatory cytokine interleukin-13 is not detectable in the circulation of multiple sclerosis patients and is not inducible by interferon-β1b treatment, that neither modifies its ex vivo secretion from peripheral blood mononuclear cells'. Together they form a unique fingerprint.

Cite this