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Srini V Kaveri - One of the best experts on this subject based on the ideXlab platform.
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Intravenous Immunoglobulin expands regulatory t cells in autoimmune rheumatic disease
The Journal of Rheumatology, 2012Co-Authors: Jagadeesh Bayry, Luc Mouthon, Srini V KaveriAbstract:To the Editor: Intravenous Immunoglobulin (IVIG) therapy can benefit diverse autoimmune and inflammatory diseases through several mutually nonexclusive mechanisms1,2. In vitro and in vivo studies in experimental models have also demonstrated that IVIG can expand CD4+CD25+ regulatory T cells (Treg), the cells that play a critical role in maintaining immune tolerance3,4. Treg maintain immune tolerance by suppressing the activation and function of both innate and adaptive immune cells, while deficiency of Treg is associated with autoimmune and inflammatory conditions5,6. Since IVIG therapy in autoimmune patients is associated with restoration of immune tolerance, we hypothesized that this effect of IVIG is in part through expansion of … Address correspondence to Dr. Bayry, INSERM U872, Equipe 16-Centre de Recherche des Cordeliers, 15 rue de l’Ecole de Medecine, Paris, F-75006, France; E-mail: jagadeesh.bayry{at}crc.jussieu.fr
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monoclonal antibody and Intravenous Immunoglobulin therapy for rheumatic diseases rationale and mechanisms of action
Nature Reviews Rheumatology, 2007Co-Authors: Jagadeesh Bayry, Michel D Kazatchkine, Sebastien Lacroixdesmazes, Srini V KaveriAbstract:Immunoglobulin-based therapies, including monoclonal antibodies and Intravenous Immunoglobulin, are effective therapeutic approaches for patients with rheumatic diseases who do not respond to conventional anti-inflammatory drugs. Several such therapies have been approved for clinical use; the mechanisms of action of these therapies are discussed in this Review. Advances in our understanding of the pathogenesis of rheumatic diseases such as rheumatoid arthritis and systemic lupus erythematosus have led to the emergence of Immunoglobulin-based therapy as a major therapeutic force. Numerous monoclonal antibodies that target proinflammatory cytokines or their receptors (e.g. infliximab, adalimumab, tocilizumab, belimumab, HuMax-IL-15), and cell-surface or co-stimulatory molecules (e.g. rituximab) are either in clinical development or have been approved for clinical use. These antibodies are safe and effective in the long-term therapy of many rheumatic diseases. In addition, polyclonal Immunoglobulins (Intravenous Immunoglobulin) obtained from pooled plasma from healthy blood donors are an effective therapeutic approach in certain rheumatic diseases. The mechanisms of action of monoclonal antibodies and Intravenous Immunoglobulin include cytolysis of target cells through complement or antibody-dependent cell-mediated cytotoxicity, induction of apoptosis of target cells, blockade of co-stimulatory molecules, and neutralization of pathogenic antibodies and soluble factors such as cytokines and their receptors, which ultimately lead to amelioration of the inflammatory process. The success of currently available therapeutic Immunoglobulins has led to considerable interest in the identification of novel molecular therapeutic targets in rheumatic diseases.
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monoclonal antibody and Intravenous Immunoglobulin therapy for rheumatic diseases rationale and mechanisms of action
Nature Reviews Rheumatology, 2007Co-Authors: Jagadeesh Bayry, Michel D Kazatchkine, Sebastien Lacroixdesmazes, Srini V KaveriAbstract:Advances in our understanding of the pathogenesis of rheumatic diseases such as rheumatoid arthritis and systemic lupus erythematosus have led to the emergence of Immunoglobulin-based therapy as a major therapeutic force. Numerous monoclonal antibodies that target proinflammatory cytokines or their receptors (e.g. infliximab, adalimumab, tocilizumab, belimumab, HuMax-IL-15), and cell-surface or co-stimulatory molecules (e.g. rituximab) are either in clinical development or have been approved for clinical use. These antibodies are safe and effective in the long-term therapy of many rheumatic diseases. In addition, polyclonal Immunoglobulins (Intravenous Immunoglobulin) obtained from pooled plasma from healthy blood donors are an effective therapeutic approach in certain rheumatic diseases. The mechanisms of action of monoclonal antibodies and Intravenous Immunoglobulin include cytolysis of target cells through complement or antibody-dependent cell-mediated cytotoxicity, induction of apoptosis of target cells, blockade of co-stimulatory molecules, and neutralization of pathogenic antibodies and soluble factors such as cytokines and their receptors, which ultimately lead to amelioration of the inflammatory process. The success of currently available therapeutic Immunoglobulins has led to considerable interest in the identification of novel molecular therapeutic targets in rheumatic diseases.
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shortage of human Intravenous Immunoglobulin reasons and possible solutions
Nature Reviews Neurology, 2007Co-Authors: Jagadeesh Bayry, Michel D Kazatchkine, Srini V KaveriAbstract:In recent years, we have witnessed an alarming worldwide shortage of Intravenous Immunoglobulin, an agent that is commonly used to treat various autoimmune and systemic inflammatory diseases, many of which affect the nervous system. In this Viewpoint, Bayryet al.explain the reasons for this shortage, and propose some potential solutions to the problem.
M Vermeulen - One of the best experts on this subject based on the ideXlab platform.
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Intravenous Immunoglobulin for multifocal motor neuropathy
Cochrane Database of Systematic Reviews, 2005Co-Authors: Ivo N. Van Schaik, Leonard H. Van Den Berg, Rob J. De Haan, M VermeulenAbstract:Background Multifocal motor neuropathy is a rare, probably immune mediated disorder characterised by slowly progressive, asymmetric, distal weakness of one or more limbs with no objective loss of sensation. It may cause prolonged periods of disability. The treatment options for multifocal motor neuropathy are sparse. Patients with multifocal motor neuropathy do not usually respond to steroids or plasma exchange, and may even worsen with these treatments. Many uncontrolled studies have suggested a beneficial effect of Intravenous Immunoglobulin. Objectives To review systematically the evidence from randomised controlled trials concerning the efficacy and safety of Intravenous Immunoglobulin in multifocal motor neuropathy. Search methods We used the search strategy of the Cochrane Neuromuscular Disease Review Group to search the Disease Group register (searched March 2007), MEDLINE (January 1990 to March 2007), EMBASE (January 1990 to March 2007) and ISI (January 1990 to March 2007) databases for randomised controlled trials. Selection criteria Randomised controlled studies examining the effects of any dose of Intravenous Immunoglobulin versus placebo in patients with definite or probable multifocal motor neuropathy. Outcome measures had to include one of the following: disability, strength, or conduction block. Studies which reported the frequency of adverse effects were used to assess safety. Data collection and analysis Two authors reviewed literature searches to identify potentially relevant trials, scored their quality and extracted data independently. For dichotomous data, we calculated relative risks, and for continuous data, effect sizes and weighted pooled effect sizes. Statistical uncertainty was expressed with 95% confidence intervals. Main results Four randomised controlled trials including a total of 34 patients were suitable for this systematic review. Strength improved in 78% of patients treated with Intravenous Immunoglobulin and only 4% of placebo-treated patients. Disability improved in 39% of patients after Intravenous Immunoglobulin treatment and in 11% after placebo (statistically not significantly different). Mild, transient side effects were reported in 71% of Intravenous Immunoglobulin treated patients. Serious side effects were not encountered. Authors' conclusions Limited evidence from randomised controlled trials shows that Intravenous Immunoglobulin has a beneficial effect on strength. There was a non-significant trend towards improvement in disability. More research is needed to discover whether Intravenous Immunoglobulin improves disability and is cost-effective.
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Intravenous Immunoglobulin for chronic inflammatory demyelinating polyradiculoneuropathy a systematic review
Lancet Neurology, 2002Co-Authors: Ivo N Van Schaik, Rob J. De Haan, John B Winer, M VermeulenAbstract:Summary This review discusses the efficacy and safety in chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) of Intravenous Immunoglobulin and compares this treatment with plasma exchange and prednisolone. We searched publications from 1985 onwards for randomised controlled studies examining the effects of Intravenous Immunoglobulin in patients with this immune-mediated neuromuscular disorder. Six trials, with 170 patients in total, were judged eligible. A significantly higher proportion of patients improved in disability within a month after the start of treatment with Intravenous Immunoglobulin than with placebo (relative risk 3·17 [95% CI 1·74 to 5·75]). During this period, Intravenous Immunoglobulin has similar efficacy to plasma exchange and oral prednisolone; therefore which of these treatments should be the first choice is currently uncertain. An algorithm on treatment approaches for CIDP is proposed.
Jagadeesh Bayry - One of the best experts on this subject based on the ideXlab platform.
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Intravenous Immunoglobulin expands regulatory t cells in autoimmune rheumatic disease
The Journal of Rheumatology, 2012Co-Authors: Jagadeesh Bayry, Luc Mouthon, Srini V KaveriAbstract:To the Editor: Intravenous Immunoglobulin (IVIG) therapy can benefit diverse autoimmune and inflammatory diseases through several mutually nonexclusive mechanisms1,2. In vitro and in vivo studies in experimental models have also demonstrated that IVIG can expand CD4+CD25+ regulatory T cells (Treg), the cells that play a critical role in maintaining immune tolerance3,4. Treg maintain immune tolerance by suppressing the activation and function of both innate and adaptive immune cells, while deficiency of Treg is associated with autoimmune and inflammatory conditions5,6. Since IVIG therapy in autoimmune patients is associated with restoration of immune tolerance, we hypothesized that this effect of IVIG is in part through expansion of … Address correspondence to Dr. Bayry, INSERM U872, Equipe 16-Centre de Recherche des Cordeliers, 15 rue de l’Ecole de Medecine, Paris, F-75006, France; E-mail: jagadeesh.bayry{at}crc.jussieu.fr
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monoclonal antibody and Intravenous Immunoglobulin therapy for rheumatic diseases rationale and mechanisms of action
Nature Reviews Rheumatology, 2007Co-Authors: Jagadeesh Bayry, Michel D Kazatchkine, Sebastien Lacroixdesmazes, Srini V KaveriAbstract:Immunoglobulin-based therapies, including monoclonal antibodies and Intravenous Immunoglobulin, are effective therapeutic approaches for patients with rheumatic diseases who do not respond to conventional anti-inflammatory drugs. Several such therapies have been approved for clinical use; the mechanisms of action of these therapies are discussed in this Review. Advances in our understanding of the pathogenesis of rheumatic diseases such as rheumatoid arthritis and systemic lupus erythematosus have led to the emergence of Immunoglobulin-based therapy as a major therapeutic force. Numerous monoclonal antibodies that target proinflammatory cytokines or their receptors (e.g. infliximab, adalimumab, tocilizumab, belimumab, HuMax-IL-15), and cell-surface or co-stimulatory molecules (e.g. rituximab) are either in clinical development or have been approved for clinical use. These antibodies are safe and effective in the long-term therapy of many rheumatic diseases. In addition, polyclonal Immunoglobulins (Intravenous Immunoglobulin) obtained from pooled plasma from healthy blood donors are an effective therapeutic approach in certain rheumatic diseases. The mechanisms of action of monoclonal antibodies and Intravenous Immunoglobulin include cytolysis of target cells through complement or antibody-dependent cell-mediated cytotoxicity, induction of apoptosis of target cells, blockade of co-stimulatory molecules, and neutralization of pathogenic antibodies and soluble factors such as cytokines and their receptors, which ultimately lead to amelioration of the inflammatory process. The success of currently available therapeutic Immunoglobulins has led to considerable interest in the identification of novel molecular therapeutic targets in rheumatic diseases.
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monoclonal antibody and Intravenous Immunoglobulin therapy for rheumatic diseases rationale and mechanisms of action
Nature Reviews Rheumatology, 2007Co-Authors: Jagadeesh Bayry, Michel D Kazatchkine, Sebastien Lacroixdesmazes, Srini V KaveriAbstract:Advances in our understanding of the pathogenesis of rheumatic diseases such as rheumatoid arthritis and systemic lupus erythematosus have led to the emergence of Immunoglobulin-based therapy as a major therapeutic force. Numerous monoclonal antibodies that target proinflammatory cytokines or their receptors (e.g. infliximab, adalimumab, tocilizumab, belimumab, HuMax-IL-15), and cell-surface or co-stimulatory molecules (e.g. rituximab) are either in clinical development or have been approved for clinical use. These antibodies are safe and effective in the long-term therapy of many rheumatic diseases. In addition, polyclonal Immunoglobulins (Intravenous Immunoglobulin) obtained from pooled plasma from healthy blood donors are an effective therapeutic approach in certain rheumatic diseases. The mechanisms of action of monoclonal antibodies and Intravenous Immunoglobulin include cytolysis of target cells through complement or antibody-dependent cell-mediated cytotoxicity, induction of apoptosis of target cells, blockade of co-stimulatory molecules, and neutralization of pathogenic antibodies and soluble factors such as cytokines and their receptors, which ultimately lead to amelioration of the inflammatory process. The success of currently available therapeutic Immunoglobulins has led to considerable interest in the identification of novel molecular therapeutic targets in rheumatic diseases.
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shortage of human Intravenous Immunoglobulin reasons and possible solutions
Nature Reviews Neurology, 2007Co-Authors: Jagadeesh Bayry, Michel D Kazatchkine, Srini V KaveriAbstract:In recent years, we have witnessed an alarming worldwide shortage of Intravenous Immunoglobulin, an agent that is commonly used to treat various autoimmune and systemic inflammatory diseases, many of which affect the nervous system. In this Viewpoint, Bayryet al.explain the reasons for this shortage, and propose some potential solutions to the problem.
Yehuda Shoenfeld - One of the best experts on this subject based on the ideXlab platform.
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idiotype specific Intravenous Immunoglobulin ivig for therapy of autoimmune diseases
Methods of Molecular Biology, 2014Co-Authors: Miri Blank, Tomer Bashi, Yehuda ShoenfeldAbstract:Intravenous Immunoglobulin (IVIG) is used successfully for therapy of inflammatory and autoimmune diseases, especially in cases of conventional therapy resistance. Within the broad spectrum of immunomodulatory activities of IVIG in vitro and in vivo, the anti-idiotypic activity, neutralizing the autoimmune disease related idiotypes, is one of the main mechanism. We and others have proven that from the IVIG composition, diverse fractions of autoimmune disease specific IVIG can be affinity purified (sIVIG). This sIVIG was shown to be more efficient than the whole compound of IVIG in experimental animal models of autoimmune diseases.The affinity purification of disease sIVIG encompasses three stages. The first stage is to construct an autoantigen column for affinity purification of the autoantibodies. In the second stage the purified autoantibodies are used to construct a new column composed of the autoantibodies. The later is utilized for affinity purification of anti-autoantibodies (anti- idiotypes) IVIG defined as autoimmune disease specific IVIG- sIVIG.
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safety of Intravenous Immunoglobulin ivig therapy
Autoimmunity Reviews, 2007Co-Authors: Uriel Katz, Yehuda Shoenfeld, Yaniv Sherer, Anat AchironAbstract:Intravenous Immunoglobulin (IVIg) is administered both for the treatment of immunodeficiencies and for an expanding list of autoimmune diseases. Most adverse effects are mild and transient including headaches, flushing, fever, chills, fatigue, nausea, diarrhea, blood pressure changes and tachycardia. IgA deficiency-related anaphylactic reactions are largely preventable. Late adverse events are rare and include acute renal failure and thromboembolic events. Acute renal failure, usually oliguric and transient, occurs generally in insufficiently hydrated patients and with sucrose-stabilized products due to osmotic injury. Thromboembolic complications occur due to hyperviscosity especially in patients having risk factors including advanced age, previous thromboembolic events, immobilization, diabetes mellitus, hypertension, dyslipidemia or those receiving high-dose IVIg in a rapid infusion rate or excessive dose. Slow infusion rate and good hydration may prevent renal failure, thromboembolic events and aseptic meningitis. In our experience in more than 200 patients receiving IVIg for different autoimmune diseases and near 10000 infusions for relapsing-remitting multiple sclerosis patients, the occurrence of adverse effects was 24-36% after high dose IVIg, most were headaches and all were mild adverse events. We conclude that IVIg is a safe therapy when given in a slow infusion rate in well-hydrated patients, better avoiding patients with known risk factors.
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Immunomodulation of experimental pulmonary fibrosis by Intravenous Immunoglobulin (IVIG).
Autoimmunity, 2006Co-Authors: Vered Molina, Saleem Haj-yahia, Inna Solodeev, Yair Levy, Miri Blank, Yehuda ShoenfeldAbstract:Objectives: To assess the immunomodulatory effect of Intravenous Immunoglobulin (IVIG) using an experimental model of bleomycin-induced pulmonary fibrosis.Methods: Pulmonary fibrosis was induced in C57BL/6 mice by direct intratracheal injection of bleomycin. Mice were treated with IVIG 1 week prior to (prevention protocol), or 10 days following bleomycin injection, when the disease was in progress. The controls used in the study included mice given phosphate buffered saline (PBS) and mice subjected to a commercial individual-IgG. Collagen-I deposits in the affected lungs were detected by Sirius red staining of paraffin embedded lung sections. The collagen-I content was measured by employing the hydroxyproline assay.Results: Prevention of bleomycin-induced pulmonary fibrosis by IVIG has been demonstrated by reduced expression of collagen-I protein in the affected lungs. The hydroxyproline levels in the lungs of the IVIG-treated mice were 214.33 ± 13.56 μg/1 g tissue, compared to the higher levels in lungs ...
Shiranee Sriskandan - One of the best experts on this subject based on the ideXlab platform.
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polyspecific Intravenous Immunoglobulin in clindamycin treated patients with streptococcal toxic shock syndrome a systematic review and meta analysis
Clinical Infectious Diseases, 2018Co-Authors: Tom Parks, Clare Wilson, Nigel Curtis, Anna Norrbyteglund, Shiranee SriskandanAbstract:We evaluated the effect of Intravenous Immunoglobulin (IVIG) on mortality in clindamycin-treated streptococcal toxic shock syndrome using a meta-analysis. In association with IVIG, mortality fell from 33.7% to 15.7% with remarkable consistency across the single randomized and four nonrandomized studies.
