Effets immunomodulateurs des immunoglobulines intraveineuses au cours des maladies auto-immunesImmunomodulatory effects of intravenous immunoglobulins (IVIg) in autoimmune diseases abstract

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Résumé

Propos. — L’effet bénéfique de l’administration des immunoglobulines intraveineuses (IgIV) a été rapporté dans un grand nombre de maladies auto-immunes, qu’elles soient associées à la mise en évidence d’auto-anticorps ou à celle de lymphocytes T autoréactifs. L’effet bénéfique des IgIV chez les malades ayant une maladie auto-immune ou inflammatoire chronique résulte de mécanismes multiples et probablement intriqués.

Points forts. — Les effets immunorégulateurs des IgIV au cours des maladies auto-immunes dépendent: de l’interaction du fragment Fc des immunoglobulines (Ig) avec les récepteurs Fc à la surface des leucocytes; de l’interaction des IgG perfusées avec les protéines du complément; de la modulation de la libération et de la synthèse des cytokines par les monocytes et lymphocytes; de la neutralisation des autoanticorps circulants; de la sélection des répertoires immunologiques; de la modulation de la prolifération cellulaire en modulant l’apoptose induite par Fas; de l’interaction des IgIV avec de nombreuses autres molécules à la surface des lymphocytes B et T.

Perspectives. — La meilleure compréhension de ces mécanismes devrait permettre de mieux définir les pathologies candidates à un traitement par les IgIV et d’optimiser leurs modalités d’administration.

Summary

Purpose. — Intravenous immunoglobulins (IVIg) therapy has been reported to be beneficial in a large number of autoantibody-mediated or self-reactive T cells-associated autoimmune diseases. Thus, the beneficial effect of IVIg is probably due to multiple distinct mechanisms.

Main points. — The immunoregulatory effect of IVIg in autoimmune diseases is dependent on: interaction of the Fc portion of IVIg with Fc receptors on leucocyte surfaces; interaction of infused IgG with complement components; modulation of synthesis and release of cytokines produced by lymphocytes and monocytes; V region-dependent neutralization of circulating autoantibodies by infused IgG; selection of immune repertoires; modulation of cell proliferation, particularity through modulation of Fas-induced apoptosis; interaction of IVIg with numerous other molecules onto the surface of T and B cells.

Perspectives. — Better understanding of these mechanisms should allow a better definition of the spectrum of diseases likely to benefit from IVIg treatment.

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