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The Role of the Complement System in Chronic Inflammatory Demyelinating Polyneuropathy: Implications for Complement-Targeted Therapies
LA. Querol, HP. Hartung, RA. Lewis, PA. van Doorn, TR. Hammond, N. Atassi, M. Alonso-Alonso, MC. Dalakas
Language English Country United States
Document type Journal Article, Review
NLK
PubMed Central
from 2007
Europe PubMed Central
from 2007 to 1 year ago
ProQuest Central
from 2007-01-01 to 2023-10-31
Nursing & Allied Health Database (ProQuest)
from 2007-01-01 to 2023-10-31
Health & Medicine (ProQuest)
from 2007-01-01 to 2023-10-31
Psychology Database (ProQuest)
from 2007-01-01 to 2023-10-31
- MeSH
- Biopsy MeSH
- Polyradiculoneuropathy, Chronic Inflammatory Demyelinating * diagnosis drug therapy MeSH
- Humans MeSH
- Macrophages pathology MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Review MeSH
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.
Brain and Mind Center University of Sydney Sydney Australia
Cedars Sinai Medical Center Los Angeles CA USA
Department of Neurology Heinrich Heine University Düsseldorf Germany
Department of Neurology Medical University of Vienna Vienna Austria
Department of Neurology Palacky University Olomouc Olomouc Czech Republic
Department of Neurology Thomas Jefferson University Hospital Philadelphia PA USA
Erasmus MC University Medical Center Rotterdam The Netherlands
Neuroimmunology National and Kapodistrian University of Athens Medical School Athens Greece
References provided by Crossref.org
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- $a 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.
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