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Research Targets Interferon Alpha in New Treatment Approach for CNS Lupus

Mary Beth Nierengarten  |  Issue: November 2017  |  November 9, 2017

Specifically, they point to the need to find the most effective way to therapeutically modulate type 1 interferon signaling in patients with lupus, particularly with the challenge of developing drugs that can cross the blood–brain barrier. They caution, however, that blocking type 1 interferon signaling in the brain is not without potential risk given the pivotal role of this pathway in host defense and the need for a basal level of interferon signaling to maintain neuronal health.”3

Dr. Tsokos says the biggest challenge will be to identify patients with CNS lupus in whom the interferon pathway is the driving force behind the symptoms & treat only those patients.

For Dr. Carroll, the promising preclinical results of anifrolumab suggest its potential as a targeted therapy in people with CNS lupus. To that end, he and his colleagues suggest that patients with CNS lupus, particularly patients with detectable interferon signatures, be included in further clinical trials of anifrolumab.1

Emphasizing that there is still much work that needs to be done to fully understand how activation of microglia by type I interferon contributes to CNS lupus symptoms, Dr. Bialas underscores the need for clinicians to document and monitor their patients for CNS lupus symptoms.

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“I think many lupus patients don’t necessarily think to discuss their neurological symptoms with their rheumatologists, and rheumatologists may not be inclined to ask about them because in most cases there aren’t lupus-specific treatments for these symptoms,” she says. That said, their research indicates new treatments may be coming up in the near future that target type I interferon.


Mary Beth Nierengarten is a freelance medical journalist based in Minneapolis.

References

  1. Bialas AR, Presumey J, Das A, et al. Microglia-dependent synapse loss in type I interferon-mediated lupus. Nature. 2017 Jun 22;546(7659):539–543.
  2. Das A, Heesters BA, Bialas A, et al. Follicular dendritic cell activation by TLR ligands promotes autoreactive b cell responses. Immunity. 2017 Jan;46(1):106–119.
  3. McGlasson S, Hunt D. Neuroinflammation: Synapses pruned in lupus. Nature. 2017 Jun 22;546(7659):482–483.
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Filed under:ConditionsResearch RheumSystemic Lupus Erythematosus Tagged with:brain dysfunctioncentral nervous systemCNS lupusinterferon alphaLupusManagementneuropsychiatricpathologyResearchrheumatologyTreatment

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