This Article Full Text (PDF) References Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Saved Citations Download to citation manager Request Permissions Request Reprints Add to My Marked Citations Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Citing Articles via Scopus Google Scholar Articles by van Schaik, I. Articles by Brand, A. Search for Related Content PubMed PubMed Citation Articles by van Schaik, I. Articles by Brand, A. Social Bookmarking                         What's this?

Immunomodulation and remyelination: two aspects of human polyclonal immunoglobulin treatment in immune mediated neuropathies?

Department of Neurology, University of Cambridge, UK, Department of Immunohematology, University Hospital Leiden, Leiden, The Netherlands

M. Vermeulen

Department of Neurology, Academic Medical Center, Amsterdam, The Netherlands

A. Brand

Department of Neurology, University of Cambridge, UK

Intravenous immunoglobulin is used in inflammatory demyelinating diseases of the peripheral as well as the central nervous system. It is not known which mechanism(s) accounts for the beneficial effect observed in these diseases. The immunomodulatory effects of IVIg in two different models of T and B cell activation were investigated. IVIg inhibited a predominantly cellular immune response of the Th 1 type, which was partially reversed by addition of Th 1 cytokines. In contrast, in a model, which leads to B cell differentiation and antibody production, a synergistic stimulatory effect of IVIg and Th2 cytokines was observed. The ability of IVIg to interfere with cell proliferation and to manipulate the Th 1/Th2 profile will have consequences for the induction, character, and amplification of an immune response. Apart from the immunomodulatory effects, evidence shows that IVIg promote remyelination not only by abrogation of the auto-immune attack but also by an effect on glial cells. We showed that IVIg induce growth arrest of normal human fibroblasts and Schwann cells. In fibroblasts this growth arrest is accompanied by upregulation of GAS-3/PMP-22 mRNA. The implications of this finding are discussed. Further studies in human Schwann cells are imperative to prove the hypothesis that IVIg directly stimulates remyelination.

Key Words: intravenous immunoglobulin • T-helper I and 2 response • cytokines • remyelination • PMP-22/GAS-3 gene

Multiple Sclerosis, Vol. 3, No. 2, 98-104 (1997)
DOI: 10.1177/135245859700300208


CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter    What's this?

This article has been cited by other articles:

				M. S. G. Kwa, I. N. van Schaik, R. R. De Jonge, A. Brand, L. Kalaydjieva, N. van Belzen, M. Vermeulen, and F. Baas Autoimmunoreactivity to Schwann cells in patients with inflammatory neuropathies Brain, February 1, 2003; 126(2): 361 - 375. [Abstract] [Full Text] [PDF]