THE INFLAMMATORY LESION OF T-CELL LINE TRANSFERRED EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS OF THE LEWIS RAT - DISTINCT NATURE OF PARENCHYMAL AND PERIVASCULAR INFILTRATES
J. Lannesvieira et al., THE INFLAMMATORY LESION OF T-CELL LINE TRANSFERRED EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS OF THE LEWIS RAT - DISTINCT NATURE OF PARENCHYMAL AND PERIVASCULAR INFILTRATES, Acta Neuropathologica, 87(5), 1994, pp. 435-442
We have investigated the T cell receptor (TCR) repertoire in the infla
mmatory infiltrates of T line-transferred experimental autoimmune ence
phalomyelitis (EAE) of the Lewis rats. Using a panel of TCR V beta-spe
cific monoclonal antibodies (mAbs) and immunocytochemistry, we studied
the nature of the T cells entering the central nervous system (CNS) a
fter transfer of either myelin basic protein (MBP)-reactive, or MBP-re
active but non-encephalitogenic T cell lines. All the MBP-specific T c
ell lines predominantely used the V beta 8.2 TCR chain. T cell lines s
pecific for the tuberculin purified protein derivative (PPD), using TC
R V genes different from V beta 8.2, served as controls. We first stud
ied the time course of T cells entering the CNS. In all recipient rats
, small, but significant numbers of alpha beta-TCR-expressing infiltra
te cells appeared in the CNS within the first 24 h after T cell transf
er. In animals injected with either type of MBP-reactive T cells, the
early infiltrate cells were preferentially located within the parenchy
ma of the spinal cord, while in PPD T line-injected rats, the lymphocy
tes were mostly found in the meninges. TCR V beta gene usage was exami
ned on the peak of clinical disease. Six days after T cell transfer, t
he TCR repertoire used by infiltrating lymphocytes in general seemed t
o be highly diverse. None of the V beta isotypes examined (i. e. V bet
a 8.2, V beta 8.5 or V beta 10) was used by a major population of the
alpha beta-TCR-positive T cells. A more detailed, quantitative analysi
s of individual infiltrate compartments revealed, however, a preferent
ial accumulation of V beta 8.2-positive T cells within the parenchyma.
In contrast, perivascular infiltrating cells used V beta genes random
ly. Our results confirm first that activated Tlymphocytes enter the br
ain rapidly irrespective. of their antigen specificity. Second, the da
ta show that most of the perivascular infiltrate T cells in the acute
EAE lesion are host-derived, recruited presumably from the recirculati
ng T cell pool, while the encephalitogenic, V beta 8.2-positive T cell
s preferentially persist within the parenchyma.