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Autor: Dalakas, Marinos C Autorita: Dalakas, Marinos C | xx0098920

3 záznamů v Medvik Filtry

Článek

The Role of the Complement System in Chronic Inflammatory Demyelinating Polyneuropathy: Implications for Complement-Targeted Therapies

Querol, Luis A
Autor Querol, Luis A Neuromuscular Diseases Unit, Department of Neurology, Hospital de La Santa Creu I Sant Pau, Barcelona, Spain
Hartung, Hans-Peter
Autor Hartung, Hans-Peter Department of Neurology, Heinrich Heine University, Düsseldorf, Germany Brain and Mind Center, University of Sydney, Sydney, Australia Department of Neurology, Medical University of Vienna, Vienna, Austria Department of Neurology, Palacky University Olomouc, Olomouc, Czech Republic
Lewis, Richard A
Autor Lewis, Richard A Cedars Sinai Medical Center, Los Angeles, CA, USA
van Doorn, Pieter A
Autor van Doorn, Pieter A Erasmus MC, University Medical Center, Rotterdam, The Netherlands
Hammond, Timothy R
Autor Hammond, Timothy R Sanofi, Neurology Clinical Development, Cambridge, MA, USA
Atassi, Nazem
Autor Atassi, Nazem Sanofi, Neurology Clinical Development, Cambridge, MA, USA
Alonso-Alonso, Miguel
Autor Alonso-Alonso, Miguel ORCID Sanofi, Neurology Clinical Development, Cambridge, MA, USA
Dalakas, Marinos C
Autor Dalakas, Marinos C ORCID Department of Neurology, Thomas Jefferson University Hospital, Philadelphia, PA, USA. Marinos.Dalakas@jefferson.edu Neuroimmunology National and Kapodistrian University of Athens Medical School, Athens, Greece. Marinos.Dalakas@jefferson.edu

Neurotherapeutics. 2022 ; 19 (3) : 864-873. [pub] 20220404

ISSN 1878-7479
Medvik
Zdroj

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.