Description
Overview
Multiple sclerosis (MS) is a chronic immune-mediated disease of the central nervous system (CNS). Despite highly effective disease-modifying therapies, disability may continue to accumulate independently of relapses and conventional MRI activity, a phenomenon increasingly recognized as progression independent of relapse activity (PIRA). PIRA is thought to reflect, at least in part, chronic CNS-compartmentalized inflammation that is only partially targeted by therapies acting on peripheral adaptive immunity.
Emerging evidence identifies CNS border tissues—including the meninges, choroid plexus, perivascular spaces, meningeal lymphatics, and skull bone marrow—as active neuroimmune interfaces involved in immune surveillance, inflammatory amplification, and tissue repair. Within these compartments, innate immune cells, particularly microglia and border-associated macrophages, appear to play a major role in chronic lesion activity and progression-related tissue damage. Their bidirectional interactions with adaptive immune cells may sustain compartmentalized inflammation and provide a link between peripheral autoimmunity and chronic CNS injury.
Within this framework, the CD40/CD40L co-stimulatory pathway represents a key molecular bridge between adaptive and innate immunity. CD40/CD40L signaling promotes B-cell and antigen-presenting cell activation, cytokine release, myeloid and microglial activation, and endothelial inflammatory responses, thereby potentially reinforcing immune-cell communication at CNS interfaces contributing to chronic CNS-compartmentalized inflammation and progression-related neurodegeneration in MS.
Learning objectives
- Discuss the evolving concept of CNS immune privilege and the role of CNS-border tissues as active neuroimmune interfaces in MS.
- Explain the mechanisms underlying immune-cell trafficking across CNS
- barriers and analyze adaptive–innate immune interactions, including microglia and border-associated macrophages, and their role in sustaining compartmentalized inflammation.
- Recognize the relevance of chronic CNS inflammation to PIRA and interpret emerging associated biomakers, including imaging, fluid, and CSF biomarkers.
- Discuss therapeutic strategies targeting neuroimmune crosstalk and chronic neuroinflammation, with particular focus on adaptive-innate immune pathways, including the CD40/CD40L axis.
- Integrate advances in neuroimmunology, imaging, and progression biology into a more comprehensive and biologically grounded approach to contemporary MS management.
Target Audience
This online Project has been carefully designed to appeal to a wide range of professionals involved in the research and treatment of MS including Neurologists, Immunologists and other HCPs engaged in the management of the disease
Accreditation
The programme will be submitted for CME accreditation to the European Accreditation Council for Continuing Medical Education (EACCME®)
Scientific Secretariat
Med-Ex Learning
Rome, Italy
Scientific Programme
Season 1: Release Date November 10th, 2026
Periphery and environment interaction
- Episode 1: Environmental triggers and origins of MS autoimmunity
Speaker to be announced
- Episode 2: Breaking the borders: immune tolerance collapse and CNS entry
R. Martin (Switzerland)
- Episode 3: Priming Neuroinflammation: Adaptive and Innate Immune Interactions
D. Baker (UK)
Season 2: Release Date December 2nd, 2026
Mapping the borders: gateways to the CNS
- Episode 1: Revisiting the concept of brain immune privilege – J. Kipnis (USA)
- Episode 2: Brain barriers as gatekeepers of neuroimmune interplay – A. Pratt (Canada)
- Episode 3: Navigating the uncharted waters: the glymphatic dysfunction in MS P. Preziosa (Italy)
Season 3: Release Date December 14th, 2026
Beyond the Borders
- Episode 1: Beneath the Surface: Compartmentalized Inflammation and Structural Damage in MS – Absinta (Italy)
- Episode 2: At the Meningeal Frontier: Inflammation and Progression Biology – R. Magliozzi (UK)
- Episode 3: Rewiring Neuroimmune Crosstalk: the CD40/CD40L Axis as an emerging Therapeutic target – G. Giovannoni (UK)