Interferon-beta responders and non-responders. A biological approach

@article{Bertolotto2008InterferonbetaRA,
  title={Interferon-beta responders and non-responders. A biological approach},
  author={Antonio Bertolotto and Francesca Gilli},
  journal={Neurological Sciences},
  year={2008},
  volume={29},
  pages={216-217}
}
The therapeutic benefits of interferon-beta are limited, as some patients with multiple sclerosis (MS) do not respond to therapy. Based on their biological characteristics, non-responsive patients can be divided into three subgroups: genetic, pharmacological and pathogenetic non-responders. In order to tailor the best treatment in both newly diagnosed MS patients and those already receiving treatment, the neurologist must carefully consider the risk of treating non-responders. 
Interferons in the Treatment of Multiple Sclerosis: A Clinical Efficacy, Safety, and Tolerability Update.
TLDR
Peginterferon beta-1a is associated with less frequent discomfort, which may translate to improved adherence, a major factor in treatment efficacy, and switching among the available interferons may be a viable option for patients who experience issues with tolerability.
Interferons in the Treatment of Multiple Sclerosis
TLDR
Peginterferon beta-1a is associated with less frequent discomfort, which may translate to improved adherence, a major factor in treatment efficacy, and switching among the available interferon therapies may be a viable option for patients who experience issues with tolerability.
Excessive Biologic Response to IFNβ Is Associated with Poor Treatment Response in Patients with Multiple Sclerosis
TLDR
It is hypothesized that the molecular response to type I IFN identifies a pathogenetically distinct subset of MS patients whose disease is driven in part by innate immunity.
Guidelines on the clinical use for the detection of neutralizing antibodies (NAbs) to IFN beta in multiple sclerosis therapy: report from the Italian Multiple Sclerosis Study group
Interferon beta (IFNβ) was the first specific disease-modifying treatment licensed for relapsing-remitting multiple sclerosis, and is still one of the most commonly prescribed treatments. A strong
β remitting multiple sclerosis treated with interferon-− Serum levels of IL-17 A in patients with relapsing
TLDR
RRMS patients with high serum IL-17A levels do not respond well to IFN-β therapy and have shorter MS duration compared to patients with low IL- 17A levels, which is not influenced by the presence of BAbs.
Association of CD58 Polymorphism with Multiple Sclerosis and Response to Interferon ß Therapy in A Subset of Iranian Population
TLDR
Investigating the frequency of rs12044852 polymorphism and its effect on the outcome of interferon beta (IFN-β) therapy in a subset of Iranian MS patients revealed the critical effect ofrs120448 52 polymorphism of CD58 on the progression of MS disease.
Serum levels of IL-17A in patients with relapsing–remitting multiple sclerosis treated with interferon-β
TLDR
RRMS patients with high serum IL-17A levels do not respond well to IFN-β therapy and have shorter MS duration compared to patients with low IL- 17A levels, which is not influenced by the presence of BAbs.
CD4+ and CD25+ T‐cell response to short‐time interferon‐beta therapy on IL10, IL23A and FOXP3 genes in multiple sclerosis patients
TLDR
The effects of interleukin 10 and 23 (IL10 and 23A), as well as forkhead box P3 (FOXP3) genes on MS after IFN‐β therapy are determined.
Challenges in randomized controlled trials and emerging multiple sclerosis therapeutics
TLDR
Recent studies using the McDonald MS diagnostic criteria carefully excluded patients with neuromyelitis optica and NMO spectrum disorder, and demonstrated that patients with MS in Asia have clinical characteristics and treatment responses similar to those in Western countries.
Monocyte NOTCH 2 expression predicts IFN-b immunogenicity in multiple sclerosis patients
TLDR
NADA development was driven by a proinflammatory environment that triggered activation of the Notch2 signaling pathway prior to first IFN-b administration, and reduced monocyte NOTCH2 expression in nADA+ MS patients was associated with increased expression of Notch-responsive genes, polarization of monocytes toward a nonclassical phenotype, and increased proinflammatory IL-6 production.
...
...

References

SHOWING 1-8 OF 8 REFERENCES
Defining the response to interferon‐β in relapsing‐remitting multiple sclerosis patients
TLDR
Various criteria of treatment response are investigated to assess which criterion better identifies patients with a poor response to interferon for multiple sclerosis.
Biological responsiveness to first injections of interferon-beta in patients with multiple sclerosis
A recommended treatment algorithm in relapsing multiple sclerosis: report of an international consensus meeting
TLDR
Treatment pathways for optimizing therapy for those patients with suboptimal responses to DMDs, and therapeutic options for patients with unacceptable side‐effects on their current therapy are suggested.
Neutralizing antibodies reduce MxA protein induction in interferon- beta-1a-treated MS patients
TLDR
Analysis of MxA protein in lymphocytes together with analysis of NAb is a promising marker for evaluating the biologic effects of IFNβ treatment in MS patients.
Neutralizing antibodies against IFN-beta in multiple sclerosis: antagonization of IFN-beta mediated suppression of MMPs.
TLDR
Findings support the concept of a significant role of NAb in reducing the therapeutic efficacy of IFN-beta and evidence that an imbalance between MMP and TIMP expression is a crucial pathogenetic feature in multiple sclerosis.
Neutralizing antibodies against IFN-β in multiple sclerosis: antagonization of IFN-β mediated suppression of MMPs
TLDR
Findings support the concept of a significant role of NAb in reducing the therapeutic efficacy of IFN-beta and suggest an imbalance between MMP and TIMP expression is a crucial pathogenetic feature in multiple sclerosis.
IL-10 receptor and coreceptor expression in quiescent and activated hepatic stellate cells.
TLDR
Concomitant induction ofIL-10R but not CRF2-4 to that of IL-10 by activated HSC in vitro and in vivo and associated acquisition of the responsiveness to IL- 10, entailing complex effects on HSC are shown.
Correlation between gene expression of interferon alpha/beta receptor and inducibility of four interferon stimulated genes in peripheral blood mononuclear cells from multiple sclerosis patients
  • Mult Scler 13[Suppl
  • 2007