Interferon-Responsive Brain Networks Identified as Potential Therapeutic Targets in MS

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“We found a very novel interaction between different cell types in the borders of the brain in this area called the meninges.”

Multiple sclerosis (MS) is driven by immune-mediated inflammation within the central nervous system. Inflammatory molecules, primarily cytokines, chemokines, and complement proteins, serve as key signaling mediators that coordinate immune cell activation, recruitment, and effector function. In MS, dysregulation of these molecules contributes to blood–brain barrier disruption, immune cell infiltration, demyelination, and neuroaxonal injury.¹

Interferons represent a particularly complex component of MS biology. Type I interferons, such as interferon-β, are established disease-modifying therapies that reduce relapse rates and inflammatory activity. In contrast, type II interferon has proinflammatory properties and has been shown to exacerbate disease activity in both experimental autoimmune encephalomyelitis models and clinical studies. This duality underscores the context-dependent role of cytokine signaling in MS pathogenesis.²

At the Americas Committee for Treatment and Research in Multiple Sclerosis (ACTRIMS) Forum 2026, held February 5 to 7, 2026, in San Diego, California, a dedicated session explored cellular and molecular mechanisms that may reshape the biological understanding of MS. Among the presenters was Anthony Filiano, PhD, associate professor of neurosurgery at Duke University in Durham, North Carolina, who delivered a presentation on inflammatory molecules, including interferons. During the session, he detailed emerging data on how interferon-responsive networks and meningeal immune interactions may contribute to early MS pathogenesis. To gain further insight, NeurologyLive® sat down with Filiano to discuss his findings.

Filiano described his lab’s efforts to better understand how the immune system conducts surveillance of the brain without triggering overt pathologic activation. In addition, he discussed the presented data identifying a novel cellular interaction within the meninges, specifically in the perivascular spaces, that appears to regulate this process at the brain’s borders. Throughout the discussion, Filiano noted that the molecular players involved in this interaction have also been implicated in genetic studies of MS, suggesting a potential role in initiating autoimmune disease. Together, he stressed that these findings point to previously unrecognized molecular mechanisms that may drive MS pathogenesis and could represent future therapeutic targets.

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REFERENCES
1. Dendrou C, Fugger L, Friese M. Immunopathology of multiple sclerosis. Nat Rev Immunol. 2015;15(9):545-558. doi:10.1038/nri3871
2. Jacobs LD, Cookfair DL, Rudick RA, et al; the Multiple Sclerosis Collaborative Research Group (MSCRG). Intramuscular interferon beta-1a for disease progression in relapsing MS. Ann Neurol. 1996;39(3):285-294. doi:10.1002/ana.410390304