Catabolism of pemphigus foliaceus autoantibodies by high-dose IVIg therapy

Aoyama, Yumi; Moriya, Chie; Nagai, Miki; Rubenstein, David; Iwatsuki, Keiji; Kitajima, Yasuo

doi:10.1684/ejd.2011.1169

Cited by 9 publications

(5 citation statements)

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“…Thus, multiple treatments will be needed if used to maintain remission. IVIg seems to act by increasing catabolism of pathogenic antibodies . It is generally well tolerated and has the attraction over other adjuvant therapies that it does not increase the risk of infection.…”

Section: Adjuvant Drugsmentioning

confidence: 99%

British Association of Dermatologists’ guidelines for the management of pemphigus vulgaris 2017

et al. 2017

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Section: Adjuvant Drugsmentioning

confidence: 99%

British Association of Dermatologists’ guidelines for the management of pemphigus vulgaris 2017

et al. 2017

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“…A targeted approach would be the selective adsorption of the IgG4 or antigen-specific antibodies, while leaving unaffected the majority of plasma IgGs, thus avoiding hypogammaglobulinemia. In addition, the removal of a very small percentage of the total IgGs could prolong the treatment effect, due to the slower rate of autoantibody reappearance after treatment ( 243 , 244 ). This could be accomplished by passing the plasma through a suitable matrix before being returned to the patient.…”

Section: Treatments Of Igg4 Neurological Diseasesmentioning

confidence: 99%

IgG4 Autoantibodies in Organ-Specific Autoimmunopathies: Reviewing Class Switching, Antibody-Producing Cells, and Specific Immunotherapies

et al. 2022

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Organ-specific autoimmunity is often characterized by autoantibodies targeting proteins expressed in the affected tissue. A subgroup of autoimmunopathies has recently emerged that is characterized by predominant autoantibodies of the IgG4 subclass (IgG4-autoimmune diseases; IgG4-AID). This group includes pemphigus vulgaris, thrombotic thrombocytopenic purpura, subtypes of autoimmune encephalitis, inflammatory neuropathies, myasthenia gravis and membranous nephropathy. Although the associated autoantibodies target specific antigens in different organs and thus cause diverse syndromes and diseases, they share surprising similarities in genetic predisposition, disease mechanisms, clinical course and response to therapies. IgG4-AID appear to be distinct from another group of rare immune diseases associated with IgG4, which are the IgG4-related diseases (IgG4-RLD), such as IgG4-related which have distinct clinical and serological properties and are not characterized by antigen-specific IgG4. Importantly, IgG4-AID differ significantly from diseases associated with IgG1 autoantibodies targeting the same organ. This may be due to the unique functional characteristics of IgG4 autoantibodies (e.g. anti-inflammatory and functionally monovalent) that affect how the antibodies cause disease, and the differential response to immunotherapies of the IgG4 producing B cells/plasmablasts. These clinical and pathophysiological clues give important insight in the immunopathogenesis of IgG4-AID. Understanding IgG4 immunobiology is a key step towards the development of novel, IgG4 specific treatments. In this review we therefore summarize current knowledge on IgG4 regulation, the relevance of class switching in the context of health and disease, describe the cellular mechanisms involved in IgG4 production and provide an overview of treatment responses in IgG4-AID.

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“…5). In a case report published by Aoyama et al, 41 1 course of 2 g/kg IVIG was able to reduce serum autoantibody concentrations (Anti-Dsg1) by 42% in a patient with pemphigus foliaceus. This 42% reduction in serum autoantibody concentrations observed in patients is within the 90% prediction window of the human PBPK model.…”

Section: Monte Carlo Simulations: Anti-fcrn Mab and Ivigmentioning

confidence: 88%

Development and Evaluation of a Physiologically Based Pharmacokinetic Model for Predicting the Effects of Anti-FcRn Therapy on the Disposition of Endogenous IgG in Humans

Balthasar

2019

Journal of Pharmaceutical Sciences

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This work scaled up a previously developed physiologically based pharmacokinetic model to predict the effects of anti-FcRn agents on the disposition of endogenous IgG in human subjects. Simulations were performed with the scaled model to predict the effects of single-and multiple-dose administration of anti-FcRn monoclonal antibodies (1-256 mg/kg) and high-dose intravenous immune globulin (0.4-2 g/ kg). The model was evaluated for prediction accuracy through comparison to the effects of rozanolixizumab, an anti-FcRn monoclonal antibodies under current clinical evaluation, on the disposition of endogenous IgG in healthy human subjects. The model provided reasonably accurate predictions of the effects of rozanolixizumab. Prediction errors for the maximum reduction in endogenous IgG concentrations were À8.50% (90% model prediction interval: À14.0% to 1.44%), 3.33% (90% model prediction interval: À13.9% to 21.2%), and 6.85% (90% model prediction interval: À35.2% to 10.5%) for rozanolixizumab doses of 1, 4, and 7 mg/kg, respectively. Model simulations predict that anti-FcRn therapies will exhibit greater dose potency in healthy volunteers than in patients with elevated IgG production rates (e.g., as typically found in autoimmune disease). The model appears to have potential for use in assessing and predicting novel dosing strategies for anti-FcRn therapies.

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Catabolism of pemphigus foliaceus autoantibodies by high-dose IVIg therapy

Cited by 9 publications

References 0 publications

British Association of Dermatologists’ guidelines for the management of pemphigus vulgaris 2017

British Association of Dermatologists’ guidelines for the management of pemphigus vulgaris 2017

IgG4 Autoantibodies in Organ-Specific Autoimmunopathies: Reviewing Class Switching, Antibody-Producing Cells, and Specific Immunotherapies

Development and Evaluation of a Physiologically Based Pharmacokinetic Model for Predicting the Effects of Anti-FcRn Therapy on the Disposition of Endogenous IgG in Humans

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