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Variability of the inhibition by total immunoglobulin of in vitro autoantibody-mediated erythrophagocytosis by mouse macrophages

  1. S. Léonard1,†,
  2. I. Pierard1,‡,
  3. T. E. Michaelsen2,
  4. S. Izui3,
  5. P. L. Masson1,
  6. J.-P. Coutelier1,*

Article first published online: 7 JUN 2006

DOI: 10.1111/j.1365-2249.2006.03107.x

Issue

Clinical & Experimental Immunology

Clinical & Experimental Immunology

Volume 145, Issue 1, pages 155–161, July 2006

Additional Information

How to Cite

Léonard, S., Pierard, I., Michaelsen, T. E., Izui, S., Masson, P. L. and Coutelier, J.-P. (2006), Variability of the inhibition by total immunoglobulin of in vitro autoantibody-mediated erythrophagocytosis by mouse macrophages. Clinical & Experimental Immunology, 145: 155–161. doi: 10.1111/j.1365-2249.2006.03107.x

Author Information

  1. 1

    Unit of Experimental Medicine, Christian de Duve Institute of Cellular Pathology, Université Catholique de Louvain, Bruxelles, Belgium,

  2. 2

    Division of Infectious Disease Control, Norwegian Institute of Public Health and School of Pharmacy, University of Oslo, Oslo, Norway, and

  3. 3

    Department of Pathology and Immunology, Centre Médical Universitaire, Université de Genève, Switzerland

  1. †

    Current address: 4845 Jalhay, Belgium.

  2. ‡

    Current address: GlaxoSmithKline SA, 1332 Rixensart, Belgium.

*J.-P. Coutelier, Unit of Experimental Medicine, ICP, 7430, Avenue Hippocrate, 74, B-1200 Bruxelles, Belgium. E-mail: coutelier@mexp.ucl.ac.be

Publication History

  1. Issue published online: 7 JUN 2006
  2. Article first published online: 7 JUN 2006
  3. Accepted for publication 26 April 2006

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Keywords:

  • autoantibodies;
  • autoimmunity;
  • macrophage;
  • phagocytosis;
  • total immunoglobulin

Summary

Several autoimmune diseases, mainly autoantibody-mediated, are attenuated by infusion of total IgG (IVIg). The efficacy varies widely from one patient to another. Using an experimental model of in vitro phagocytosis of autoantibody-coated erythrocytes by mouse macrophages, we analysed the possible causes for such a variability. Our results indicated that the efficacy of the phagocytosis inhibition depends upon different factors, such as the isotype and the extent of polymerization of the immunoglobulin used for the treatment as well as the genetic background of the mice and the state of macrophage activation that can be influenced by concomitant viral infection. The development of an in vitro assay for the phagocytic activity of macrophages might improve the selection of patients susceptible to benefit from IVIg treatment.

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