NON-NEURAL-SPECIFIC T-LYMPHOCYTES CAN ORCHESTRATE INFLAMMATORY PERIPHERAL NEUROPATHY

Citation
Gk. Harvey et al., NON-NEURAL-SPECIFIC T-LYMPHOCYTES CAN ORCHESTRATE INFLAMMATORY PERIPHERAL NEUROPATHY, Brain, 118, 1995, pp. 1263-1272
Citations number
53
Categorie Soggetti
Neurosciences,"Clinical Neurology
Journal title
BrainACNP
ISSN journal
00068950
Volume
118
Year of publication
1995
Part
5
Pages
1263 - 1272
Database
ISI
SICI code
0006-8950(1995)118:<1263:NTCOIP>2.0.ZU;2-K
Abstract
Neural-specific T lymphocytes are held to play a pathological role in inflammatory peripheral nerve disorders such as the Guillain-Barre syn drome (GBS) and chronic inflammatory demyelinating polyneuropathy (CID P). Here, non-neural-specific 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 ovalbu min. Rapid endoneurial perivenular infiltration of alpha beta T cells and ED1(+) macrophages occurred with ovalbumin injection following tra nsfer of 2X10(6) T cells. This cellular infiltration and accumulation produced marked increases in blood-nerve barrier (BNB) permeability. I n contrast, control casein injections produced neither significant cel l accumulation nor BNB permeability changes. Transfer of a higher numb er of T cells (5X10(6)) induced severe Wallerian degeneration and nerv e conduction failure in ovalbumin injected nerves. Fewer T cells (5X10 (5)) induced conduction block and mild demyelination which were marked ly augmented by systemic cotransfer of anti-myelin immunoglobulin. Thi s study demonstrates that activated T cells of non-neural specificity can accumulate in peripheral nerve, produce dramatic changes in BNB pe rmeability and with intravenous anti-myelin antibody orchestrate prima ry demyelination or axonal degeneration in a dose-dependent fashion.