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[Mechanisms of action of intravenous immunoglobulins in the treatment of autoimmune diseases].

Luc Mouthon, Hurez, M Kazatchkine

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Abstract

Administration of intravenous immunoglobulins (IVIg) has been reported to be beneficial in a large number of autoimmune diseases, whether mediated by autoantibodies or by T cells. Immunoregulatory effect of IVIg in autoimmune diseases is dependent on the interaction of the Fc portion of IVIg with Fc receptor on leukocytes and on the selection of recipient's immune repertoires by variable (V) regions of infused immunoglobulins. Thus: a) IVIg contains antibodies reactive with idiotypes of natural and disease-related autoantibodies and surface immunoglobulins of B cells; IVIg also contains antibodies reactive with idiotype, framework and constant regions of the beta chain of the T cell receptor; b) infusion of IVIg results in transient or long lasting suppression of specific autoantibody clones in vivo; c) infusion of IVIg alters the general "architecture" of the network as assessed by studying the kinetic patterns of spontaneous fluctuations of natural autoantibodies in serum; d) infusion of IVIg results in a modulation of synthesis and release of cytokines. This review points out mechanisms of action of IVIg in autoimmune and inflammatory diseases, focussing on those depending on V region of infused immunoglobulins.

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What this paper is about

Administration of intravenous immunoglobulins (IVIg) has been reported to be beneficial in a large number of autoimmune diseases, whether mediated by autoantibodies or by T cells. Immunoregulatory effect of IVIg in autoimmune diseases is dependent on the interaction of the Fc portion of IVIg with Fc receptor on leukocytes and on the selection of recipient's immune repertoires by variable (V) regions of infused immunoglobulins. Thus: a) IVIg contains antibodies reactive with idiotypes of natural and disease-related autoantibodies and surface immunoglobulins of B cells; IVIg also contains antibodies reactive with idiotype, framework and constant regions of the beta chain of the T cell receptor; b) infusion of IVIg results in transient or long lasting suppression of specific autoantibody clones in vivo; c) infusion of IVIg alters the general "architecture" of the network as assessed by studying the kinetic patterns of spontaneous fluctuations of natural autoantibodies in serum; d) infusion of IVIg results in a modulation of synthesis and release of cytokines. This review points out mechanisms of action of IVIg in autoimmune and inflammatory diseases, focussing on those depending on V region of infused immunoglobulins.

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Available abstract

Administration of intravenous immunoglobulins (IVIg) has been reported to be beneficial in a large number of autoimmune diseases, whether mediated by autoantibodies or by T cells. Immunoregulatory effect of IVIg in autoimmune diseases is dependent on the interaction of the Fc portion of IVIg with Fc receptor on leukocytes and on the selection of recipient's immune repertoires by variable (V) regions of infused immunoglobulins. Thus: a) IVIg contains antibodies reactive with idiotypes of natural and disease-related autoantibodies and surface immunoglobulins of B cells; IVIg also contains antibodies reactive with idiotype, framework and constant regions of the beta chain of the T cell receptor; b) infusion of IVIg results in transient or long lasting suppression of specific autoantibody clones in vivo; c) infusion of IVIg alters the general "architecture" of the network as assessed by studying the kinetic patterns of spontaneous fluctuations of natural autoantibodies in serum; d) infusion of IVIg results in a modulation of synthesis and release of cytokines. This review points out mechanisms of action of IVIg in autoimmune and inflammatory diseases, focussing on those depending on V region of infused immunoglobulins.

Key concepts: Autoantibody, Medicine, Antibody, Idiotype, Immunology, Autoimmune disease, Autoimmunity, Immune system

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[Mechanisms of action of intravenous immunoglobulins in the treatment of autoimmune diseases]. — Research Paper | ScholarLens