Immunoadsorption therapy and complement activation

Pták, Jan; Lochman, Jan

doi:10.1016/j.transci.2004.07.014

Cited by 8 publications

(7 citation statements)

References 6 publications

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“…The associated reduction in circulating C3 levels in mice receiving ND-AChR may be explained by the removal of circulating immune complexes or may indicate a concomitant inhibition in complement system reactivity. A similar effect has been reported in MG patients receiving extracorporeal immunoadsorption (Ptak and Lochman, 2005). …”

Section: Discussionsupporting

confidence: 84%

In vivo adsorption of autoantibodies in myasthenia gravis using Nanodisc-incorporated acetylcholine receptor

Sheng

Grimme²,

Bhattacharya

et al. 2010

Experimental Neurology

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Autoantibodies directed against the skeletal muscle acetylcholine receptor (AChR) play a critical role in the pathogenesis of the autoimmune disease, myasthenia gravis (MG). The pathogenic importance of anti-AChR antibodies is substantiated clinically by the often dramatic clinical improvement that follows removal of circulating antibodies utilizing extracorporeal plasma exchange (PE). Unfortunately, the effects of PE are non-specific as immunoglobulins (IgG) and other plasma proteins are removed in addition to anti-AChR IgG. In this study, we have successfully incorporated the AChR protein purified from Torpedo Californicus into a Nanodisc (ND) membrane scaffold protein/phospholipid structure. We go on to demonstrate the effectiveness of this ND-AChR complex, administered intravenously, in the in vivo down-modulation of anti-AChR antibodies and subsequent amelioration of clinical disease in the experimental murine model of MG. These results provide proof-of-principle for the in vivo antigen-specific reduction of pathogenic anti-AChR antibodies utilizing ND-AChR particles. Further development of this strategy may provide an effective, antigen-specific, and readily accessible acute therapy for exacerbating MG or myasthenic crisis.

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Section: Discussionsupporting

confidence: 84%

In vivo adsorption of autoantibodies in myasthenia gravis using Nanodisc-incorporated acetylcholine receptor

Sheng

Grimme²,

Bhattacharya

et al. 2010

Experimental Neurology

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“…Notably, in most of these studies, clinical amelioration was paralleled with reduction of NMJ MAC deposits and normal muscle AChR content despite the presence of IgG deposits at the NMJ, suggesting that AChR antibodies are not capable of inducing NMJ damage without the aid of the complement system. In a similar fashion to EAMG studies, improvement of MG symptoms following intravenous immunoglobulin (IVIg) treatment or plasma exchange has invariably been shown to be associated with a decrease in serum C3 and/ or C4 levels [26].…”

Section: Complement System In Achr Antibody Positive Mg and Eamgmentioning

confidence: 85%

Complement and cytokine based therapeutic strategies in myasthenia gravis

Tüzün

Huda

Christadoss

2011

Journal of Autoimmunity

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“…Routine examinations of C3 concentrations were done by nephel-ometry. 16 Briefly, 96-well microtiter plates (Eppendorf, Hamburg, Germany) were covered with goat antibody to human C3 (Complement Technology, Tyler, Texas) at 4 C overnight. The plates were blocked with 2% bovine serum albumin in phosphate-buffered saline (PBS) at room temperature for 30 min.…”

Section: Dtiter ¼mentioning

confidence: 99%

Correlation of C3 level with severity of generalized myasthenia gravis

et al. 2009

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Acute exacerbation of generalized myasthenia gravis (GMG) can cause swallowing impairment, respiratory failure, or death. It is important to identify immunological factors that might be regarded reliably as an index of the patient's clinical condition, response to treatment, and measure of certain immune aberrations of MG. In this study we investigated correlations between complement component C3, acetylcholine receptor antibody (AChRab) titer, and clinical severity of GMG. AChRab titer and C3 concentration were determined by radioimmunoassay and nephelometry, respectively. The clinical severity of GMG was assessed by the quantitative MG score (QMGS) according to Besinger and colleagues. Our findings indicate that the C3 level correlates with clinical severity of AChRab-positive GMG.

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Immunoadsorption therapy and complement activation

Cited by 8 publications

References 6 publications

In vivo adsorption of autoantibodies in myasthenia gravis using Nanodisc-incorporated acetylcholine receptor

In vivo adsorption of autoantibodies in myasthenia gravis using Nanodisc-incorporated acetylcholine receptor

Complement and cytokine based therapeutic strategies in myasthenia gravis

Correlation of C3 level with severity of generalized myasthenia gravis

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