Brain, Vol. 118, No. 5, 1263-1272, 1995
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Non-neural-specific T lymphocytes can orchestrate inflammatory peripheral neuropathy
1Institute of Clinical Neurosciences, Department of Medicine, University of Sydney Australia 2Neurologische Klinik, Bayerische Julius-Maximilians-Universität, Würzburg Germany
Correspondence to:
Dr G. K. Harvey, Institute of Clinical Neurosciences, Department of Medicine, University of Sydney, NSW 2006, Australia
Neural-specific T lymphocytes are held to play a pathological role in inflammatory peripheral nerve disorders such as the Guillain—Barré syndrome (GBS) and chronic inflammatory demyelinating polyneuropathy (CIDP). Here, non-neuralspecific T-cell-mediated inflammation was studied in peripheral nerves in Lewis rats by systemic transfer of ovalbumin-specific activated T cells followed by intraneural injection of ovalbumin. Rapid endoneurial perivenular infiltration of 
ß T cells and EDI+ macrophages occurred with ovalbumin injection following transfer of 2x106 T cells. This cellular infiltration and accumulation produced marked increases in blood—nerve barrier (BNB) permeability. In contrast, control casein injections produced neither significant cell accumulation nor BNB permeability changes. Transfer of a higher number of T cells (5x106) induced severe Wallerian degeneration and nerve conduction failure in ovalbumin injected nerves. Fewer T cells (5x105) induced conduction block and mild demyelination which were markedly augmented by systemic cotransfer of anti-myelin immunoglobulin. This study demonstrates that activated T cells of non-neural specificity can accumulate in peripheral nerve, produce dramatic changes in BNB permeability and with intravenous anti-myelin antibody orchestrate primary demyelination or axonal degeneration in a dose-dependent fashion.
anti-myelin; blood-nerve barrier; bystander demyelination; peripheral nerve; T lymphocyte
Received September 22, 1994. Revised April 13, 1995. Accepted May 8, 1995.
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