The Role of the Complement System in Chronic Inflammatory Demyelinating Polyneuropathy

Chronic inflammatory demyelinating polyneuropathy (CIDP) is the most common, heterogeneous, immune-mediated neuropathy, characterized by predominant demyelination of motor and sensory nerves. CIDP follows a relapsing-remitting or a progressive course and causes substantial disability. The pathogenes...

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Detalles Bibliográficos
Autores: Querol, Luis|||0000-0002-4289-8264, Hartung, Hans-Peter|||0000-0002-0614-6989, Lewis, Richard A., van Doorn, Pieter A., Hammond, Timothy R., Atassi, Nazem, Alonso-Alonso, Miguel|||0000-0003-3372-9933, Dalakas, Marinos C.
Tipo de recurso: artículo
Fecha de publicación:2022
País:España
Institución:Universitat Autònoma de Barcelona
Repositorio:Dipòsit Digital de Documents de la UAB
Idioma:inglés
OAI Identifier:oai:ddd.uab.cat:286323
Acceso en línea:https://ddd.uab.cat/record/286323
https://dx.doi.org/urn:doi:10.1007/s13311-022-01221-y
Access Level:acceso abierto
Palabra clave:CIDP
Complement inhibition
Complement system
Demyelination
Pathogenesis
Peripheral neuropathy
Descripción
Sumario:Chronic inflammatory demyelinating polyneuropathy (CIDP) is the most common, heterogeneous, immune-mediated neuropathy, characterized by predominant demyelination of motor and sensory nerves. CIDP follows a relapsing-remitting or a progressive course and causes substantial disability. The pathogenesis of CIDP involves a complex interplay of multiple aberrant immune responses, creating a pro-inflammatory environment, subsequently inflicting damage on the myelin sheath. Though the exact triggers are unclear, diverse immune mechanisms encompassing cellular and humoral pathways are implicated. The complement system appears to play a role in promoting macrophage-mediated demyelination. Complement deposition in sural nerve biopsies, as well as signs of increased complement activation in serum and CSF of patients with CIDP, suggest complement involvement in CIDP pathogenesis. Here, we present a comprehensive overview of the preclinical and clinical evidence supporting the potential role of the complement system in CIDP. This understanding furnishes a strong rationale for targeting the complement system to develop new therapies that could serve the unmet needs of patients affected by CIDP, particularly in those refractory to standard therapies.