Research paperComplement depletion affects demyelination and inflammation in experimental allergic neuritis☆
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Cited by (45)
Serum C3 complement levels predict prognosis and monitor disease activity in Guillain-Barré syndrome
2023, Journal of the Neurological SciencesCitation Excerpt :Eculizumab, an anti-C5 therapy, has been approved to treat seropositive generalized myasthenia gravis and neuromyelitis optica [21,22]. In GBS, the pathogenic role of complements and the potential benefit of inhibiting them have been observed in ganglioside or myelin-immunized murine models and in a preliminary clinical trial [23–29]. However, few studies have investigated the use of complement proteins as prognostic or monitoring biomarkers in GBS [30,31].
Ultrastructural characterization of mitochondrial damage in experimental autoimmune neuritis
2020, Journal of NeuroimmunologyCitation Excerpt :These pathological changes were not closely associated with the clinical course but with tissue injury, since they could also be detected (along with onion bulb formation even in higher frequency) when animals were already recovering (d28). Our histological data and previous studies (Kadlubowski et al., 1980; Rosen et al., 1990; Vriesendorp et al., 1995) clearly demonstrate that EAN is primarily a model of immune-mediated demyelination rather than axonal degeneration. Thus, swollen mitochondria in Schwann cells may therefore be a morphological correlate of their damage and subsequent demyelination as demonstrated in other neuropathic conditions such as diabetic or toxic neuropathy (Anderson et al., 1994; Kalichman et al., 1998).
Macrophage biology in the peripheral nervous system after injury
2019, Progress in NeurobiologyCitation Excerpt :Complement can be depleted by intravenous administration of cobra venom factor. When the sciatic nerve was crushed a day later, a reduction of CD68+ macrophage accumulation was seen in the distal nerve segment (Dailey et al., 1998; Vriesendorp et al., 1998, 1995, 1997). Complement-depleted animals showed decreased myelin clearance and decreased sciatic nerve regeneration (Dailey et al., 1998).
Tissue resident macrophages are sufficient for demyelination during peripheral nerve myelin induced experimental autoimmune neuritis?
2017, Journal of NeuroimmunologyCitation Excerpt :After intraneural injection the pathology was distinctive as antibodies in the rabbit anti-myelin sera induced myelin splitting and vacuolation that was correlated with conduction block (Saida et al., 1980) in the absence of inflammation. Activation of complement is also necessary for demyelination to occur as depletion of complement component C3 using cobra venom or C3b and C4b using sCR1 greatly reduces the severity of PNM induced EAN (Feasby et al., 1987; Jung et al., 1995; Vriesendorp et al., 1995). Membrane attack complex (MAC) staining on the surface of myelin has been observed during the onset of EAN in Lewis rats and this suggested a direct role for membrane attack complex during the initial stages of demyelination (Stoll et al., 1991).
Innate immunity in the nervous system
2009, Progress in Brain ResearchCitation Excerpt :Decomplementation is achieved via the consumption of C3 by the CVF-fB convertase. Systemic complement depletion with CVF significantly reduces inflammation and demyelination in the EAN and adoptive transfer-EAN (AT-EAN) models of GBS (Vriesendorp et al., 1995). However, the massive C activation associated with decomplementation, makes CVF a potential threat for the development of iatrogenic shock syndrome as already observed in some animal models (Younger et al., 2001).
The complement system in the peripheral nerve: Friend or foe?
2008, Molecular Immunology
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Presented at the Peripheral Nerve Society meeting, Minneapolis, June 1994.