The FcRgamma chain is not essential for induction of experimental allergic encephalomyelitis (EAE) or anti-myelin antibody-mediated exacerbation of EAE.
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Summary
The role of FcgammaR and anti-myelin antibodies in MOG35-55-induced experimental allergic encephalomyelitis (EAE) in C57BL/6 mice is studied, demonstrating that the FcRy chain is not essential for induction of EAE, but that FcRgamma signaling may contribute to the preclinical phase.
- Type
- article
- Published
- 2005-04-01
- Cited by
- 16
- References
- 68
- Access
- Open access
- OpenAlex
- https://openalex.org/W205888136
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:13205250
Keywords
Experimental autoimmune encephalomyelitis, Immunology, Proteolipid protein 1, Antibody, Myelin
References
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- Cutting Edge: Both Activating and Inhibitory Fc Receptors Expressed on Mast Cells Regulate Experimental Allergic Encephalomyelitis Disease Severity 1
- Roles of Fc receptors in autoimmunity
- The demyelinating potential of antibodies to myelin oligodendrocyte glycoprotein is related to their ability to fix complement.
- Cutting Edge: C3, a Key Component of Complement Activation, Is Not Required for the Development of Myelin Oligodendrocyte Glycoprotein Peptide-Induced Experimental Autoimmune Encephalomyelitis in Mice1
- The MHC Class I-Like IgG Receptor Controls Perinatal IgG Transport, IgG Homeostasis, and Fate of IgG-Fc-Coupled Drugs1
- IgG Fc receptors.
- G-CSF Therapy of Ongoing Experimental Allergic Encephalomyelitis Via Chemokine- and Cytokine-Based Immune Deviation
- Induction of arthritis by single monoclonal IgG anti‐collagen type II antibodies and enhancement of arthritis in mice lacking inhibitory FcγRIIB
- Role of Fc receptor gamma-chain in platelet glycoprotein Ib-mediated signaling.
- Disruption of the C5a receptor gene fails to protect against experimental allergic encephalomyelitis
- Complement-receptor-3 and scavenger-receptor-AI/II mediated myelin phagocytosis in microglia and macrophages.
- FcR gamma chain deletion results in pleiotrophic effector cell defects.
- FcgammaRI (CD64) contributes substantially to severity of arthritis, hypersensitivity responses, and protection from bacterial infection.
- Reactive microglia in multiple sclerosis lesions have an increased expression of receptors for the Fc part of IgG.
- Fc receptors are major mediators of antibody based inflammation in autoimmunity.
- Modulation of blood-brain barrier dysfunction and neurological deficits during acute experimental allergic encephalomyelitis by the N-methyl-D-aspartate receptor antagonist memantine.
- CD3+CD16+NK1.1+B220+ large granular lymphocytes arise from both alpha- beta TCR+CD4-CD8- and gamma-delta TCR+CD4-CD8- cells
Cited by
- Plasma Factors as Endogenous Agonists and Modulators of TLR4 Signaling in Microglia
- Soluble helminth products suppress clinical signs in murine experimental autoimmune encephalomyelitis and differentially modulate human dendritic cell activation.
- Relevance of anti-myelin antibodies in Multiple Sclerosis
- Myelin flow cytometry assay detects enhanced levels of antibodies to human whole myelin in a subpopulation of multiple sclerosis patients.
- The NR1 subunit of NMDA receptor regulates monocyte transmigration through the brain endothelial cell barrier
- ITAM signaling in dendritic cells controls T helper cell priming by regulating MHC class II recycling.
- Immunosuppressive monoclonal antibody to CD64 from patients with long-term stable multiple sclerosis.
- IgG glycan hydrolysis by EndoS inhibits experimental autoimmune encephalomyelitis
- Post-translational modifications of myelin oligodendrocyte glycoprotein in CNS autoimmunity
- Anti-CD48 mAb attenuates experimental autoimmune encephalomyelitis by limiting the number of pathogenic CD4+ T cells
- In vivo insights into the pathogenesis of demyelinaton in multiple sclerosis and its animal model
- Myelin oligodendrocyte glycoprotein-specific antibodies from multiple sclerosis patients exacerbate disease in a humanized mouse model.
- The emerging role of microglia in the development and therapy of multiple sclerosis.
- The role of C-reactive protein in arthritic disease
- regulating MHC class II recycling ITAM signaling in dendritic cells controls T helper cell priming by
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