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.