Brain, Vol. 115, No. 6, 1633-1646, 1992
© 1992 Guarantors of Brain
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TRANSIENT CELLULAR EXPRESSION OF 
-INTERFERON IN MYELIN-INDUCED AND T-CELL LINE-MEDIATED EXPERIMENTAL AUTOIMMUNE NEURITIS
1Department of Neurology, Heinrich-Heine-Universitât, Düsseldorf Würzburg, Germany 2Department of Neurology Julius-Maximilians-Universitât Würzburg, Germany 3TNO Institute of Applied Radiobiology and Immunology Rijswijk, The Netherlands
Correspondence to:
Correspondence to: Guido Stoll, MD, Department of Neurology, Heinrich-Heine-Universität, Moorenstr. 5, D-4000 Düsseldorf, Germany.
This study reports the cellular localization of 
-interferon (-IFN) in nerve roots during the course of experimental autoimmune neuritis induced either by active immunization (EAN) or adoptive transfer of P2-specific T-cells (AT-EAN). One micrometre thick cryosections of ventral roots of EAN and AT-EAN animals were labelled with the monoclonal antibodies DB-1 and DB-12 recognizing different epitopes of rat -IFN. In EAN numerous -IFN-positive cells were present before overt clinical signs and demyelination (days 11 - 13 after immunization). Concomitantly, raised -IFN levels were measured in the serum of these animals. However, systemically increased -IFN serum levels were not specific for a neuritogenic T-cell response. At subsequent stages when many axons were demyelinated (day 16 and later) -IFN-positive cells had disappeared and -IFN serum levels returned to normal value. -Interferon positive cells could be identified as W3/13 positive T-cells and polymorphonuclear leukocytes. Additionally, a considerable number of EDI-positive macrophages showed -IFN immunoreactivity. The majority of macrophages and all Schwann cells were -IFN negative. Similar results were obtained in AT-EAN 4 d and 6 d following cell transfer. After nerve transection no -IFN-positive cells were found in the distal stumps. The localization of -IFN in nerve roots indicates an important role of this lymphokine in acute immune-mediated demyelination. -Interferon most likely locally affects macrophage functions such as migration, major histocompatibility complex (MHC) class II antigen (Ia) expression, and production of cytotoxic molecules in nerves, and thereby contributes to myelin damage.
Received August 29, 1991. Revised June 8, 1992. Accepted June 14, 1992.
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