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In Vitro Differentiation of Naive CD4+ T Cells into Pathogenic Th17 Cells in Mouse
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Interferon-β exacerbates Th17-mediated inflammatory disease

Robert C Axtell1, Chander Raman, Lawrence Steinman

  • 1Department of Neurology and Neurological Sciences, Stanford University, Stanford, CA 94305, USA. axterobe@stanford.edu

Trends in Immunology
|May 3, 2011
PubMed

Insights

Interferon-beta (IFN-β) is a common multiple sclerosis (MS) treatment, but many patients do not respond. A prominent Th17 immune response indicates IFN-β ineffectiveness and potential harm in diverse diseases.

Area of Science:

  • Immunology
  • Neurology
  • Autoimmune Diseases

Background:

  • Interferon-beta (IFN-β) is a primary treatment for relapsing-remitting multiple sclerosis (RRMS).
  • A significant percentage of MS patients (30-50%) exhibit non-responsiveness to IFN-β.
  • IFN-β can exacerbate MS symptoms and consistently worsens neuromyelitis optica (NMO).

Purpose of the Study:

  • To identify biomarkers predicting IFN-β treatment outcomes in RRMS and other diseases.
  • To avoid ineffective treatments and potential harm from IFN-β.
  • To elucidate the mechanisms underlying IFN-β response and non-response.

Main Methods:

  • Analysis of human samples from patients with RRMS, NMO, psoriasis, rheumatoid arthritis, systemic lupus erythematosus, and ulcerative colitis.
  • Investigation of immune response profiles, specifically focusing on T helper 17 (Th17) cells.

Main Results:

  • A prominent Th17 immune response was identified as a predictor of IFN-β ineffectiveness.
  • This Th17-dominant immune response is associated with poor clinical outcomes in diverse autoimmune conditions.
  • Biomarker discovery offers potential for personalized treatment strategies.

Conclusions:

  • The presence of a strong Th17 immune response suggests that IFN-β is likely to be ineffective and may worsen disease.
  • Identifying Th17 dominance as a biomarker can guide treatment decisions, improving patient outcomes.
  • This finding has implications for managing multiple sclerosis and other immune-mediated diseases.

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