Suppression of Autoimmunity through Manipulation of Immune Network with Normal Immunoglobulin G

Kaveri, Srini V.; Dietrich, Gilles; Ronda, Nicoletta; Hurez, Vincent; Souza, Valéria Ruiz de; Rowen, Daniel; Vassilev, Tchavdar; Kazatchkine, M. D.

doi:10.1007/978-3-642-51479-1_83

Cited by 2 publications

(2 citation statements)

References 18 publications

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“…11 These include the blockade of Fc␥ receptors on phagocytic cells, 27 interference with activated complement, 28,29 modulation of production and release of cytokines and their inhibitors, 30,31 modulation of T-and B-lymphocyte functions, [32][33][34] suppression of autoantibody production, and selection of immune repertoires. 35,36 However, little is known on the direct interaction between IVIg and ECs of the vascular bed. The present study was undertaken to address the potential role of IVIg on EC function by following both EC proliferation and EC expression of key adhesion molecules, chemokines, and cytokines.…”

Section: Thus Blockade Of Cellular Proliferation and Of Cytokine-inmentioning

confidence: 99%

Modulation of Endothelial Cell Function by Normal Polyspecific Human Intravenous Immunoglobulins

Poirier

Huyen

et al. 1998

The American Journal of Pathology

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Intravenous immunoglobulin (IVIg) is increasingly used in the treatment of autoimmune and inflammatory diseases, including vasculitides and Kawasaki disease. However, the outcome of IVIg interaction with endothelial cells of the vascular bed is not clear as yet. We have investigated the effect of IVIg on the in vitro activation of human endothelial cells, as assessed by cell proliferation and reverse transcription-polymerase chain reaction-detected expression of mRNA coding for adhesion molecules (intercellular adhesion molecule-1 and vascular cellular adhesion molecule-1), chemokines (monocyte chemoattractant protein-1, macrophage colony-stimulating factor, and granulocyte-macrophage colony-stimulating factor), and proinflammatory cytokines (tumor necrosis factor-alpha, interleukin-1beta, and interleukin-6). IVIg inhibited proliferation of endothelial cells in a time-dependent manner. This effect was dependent on both Fc and F(ab')2 fragments of the immunoglobulin molecule and was fully reversible. Tumor necrosis factor-alpha and interleukin-1beta also inhibited thymidine incorporation, but to a lesser degree. IVIg had no effect on basal levels of mRNA coding for the adhesion molecules, chemokines, and proinflammatory cytokines. IVIg fully down-regulated the expression induced by tumor necrosis factor-alpha or interleukin-1beta of mRNA coding for these molecules. Thus, blockade of cellular proliferation and of cytokine-induced expression of adhesion molecules, chemokines, and cytokines may explain the therapeutic effect of IVIg in vascular and inflammatory disorders.

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Section: Thus Blockade Of Cellular Proliferation and Of Cytokine-inmentioning

confidence: 99%

Modulation of Endothelial Cell Function by Normal Polyspecific Human Intravenous Immunoglobulins

Poirier

Huyen

et al. 1998

The American Journal of Pathology

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“…The immunoregulatory role of IVIg in autoimmune disease is critically dependent on the variable regions of infused IgG [31]. The presence of antibodies to the CDS molecule in IVIg may thus have implications for the regulatory effect of IVIg in autoimmune diseases.…”

Section: Discussionmentioning

confidence: 99%

Antibodies to the CD5 molecule in normal human immunoglobulins for therapeutic use (intravenous immunoglobulins, IVIg)

Vassilev

Gélin

Kaveri

et al. 1993

Clinical and Experimental Immunology

117

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SUMMARYTVIg are increasingly used Tor the treatment of autoimmune diseases. In the present study, we show thai IVIg contain antibodies directed againsl CD5. a cell surface molecule ofT cells which is also a marker of the auloantibody-producing CD20'('B The CD5 molecule is a 67-kD glycoprotein expressed on ihymoeytes and on the majority of mature T lymphocytes. The CD5 molecule is also found on a subpopulation of B cells [8] eonsliluting ihc majority of B lymphocytes of the newborn, and accounting for IO-3O' !<> of circulating tonsillar and splenic B lymphocytes [9][10][11]. CD5' B cells in cord blood and EpsteinBarr virus (EBV)-transformed peripheral blood B lymphocytes from healthy donors produce "natural' autoantibodies that are Correspondence: Michel D, Kazatchkinc, INSERM U28. Hopitai Broussats, Paris, France. autoreactive and polyspecifie [12]. There is evidence that CDS* B cells are increased in numbers and produce autoantibodies in patients wilh rheumatoid arthritis, systemic lupus erythematosus and Sjogren's syndrome [13][14][15]. In addition, chronic lymphocytic leukaemia B cells express CD5 [16] and produce autoantibodies which exhibit the genetic and functional characteristics of the natural antibodies produced in healthy individuals [17],-In the present study, we demonstrate that therapeutic IVIg preparations contain antibodies lo ihe CD5 molecule. The presence of CDS antibodies in IVIg may have implications for the immunoregulatory effects of normal immunoglobulins on seleetion and expression of autoimmune repertoires.

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Suppression of Autoimmunity through Manipulation of Immune Network with Normal Immunoglobulin G

Cited by 2 publications

References 18 publications

Modulation of Endothelial Cell Function by Normal Polyspecific Human Intravenous Immunoglobulins

Modulation of Endothelial Cell Function by Normal Polyspecific Human Intravenous Immunoglobulins

Antibodies to the CD5 molecule in normal human immunoglobulins for therapeutic use (intravenous immunoglobulins, IVIg)

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