Ma. Jensen et al., GLOBAL INHIBITION OF IL-2 AND IFN-GAMMA SECRETING T-CELLS PRECEDES RECOVERY FROM ACUTE MONOPHASIC EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS, Journal of autoimmunity, 9(5), 1996, pp. 587-597
Actively induced experimental autoimmune encephalomyelitis (EAE) in th
e PL/J mouse is a monophasic disease. We isolated mononuclear cells (M
NC) from the central nervous system (CNS), lymph node (LN), blood, and
spleen over the course of EAE and counted the number of cells secreti
ng IL-2, IFN-gamma or IL-4 in response to polyclonal stimulation. IL-2
secreting cells were present in the CNS at disease onset but absent a
t disease peak and at recovery. A profound transient drop in IL-2 secr
eting cells also occurred in LN, blood, and spleen at disease peak and
during recovery. IFN-gamma secreting cell number decreased in all com
partments as disease evolved. In contrast, IL-4 secreting cell number
was greatest in the CNS at disease peak, i.e. IL-4 secreting cells ros
e as IL-2 and IFN-gamma secreting cells fell. IL-4 secreting cell numb
er did not change appreciably in LN, blood, and splenic MNC as disease
evolved. CNS MNC at disease peak failed to proliferate in response to
anti-CD3 mAb but did so in response to IL-2. LN, blood and splenic MN
C did proliferate in response to anti-CD3 mAb at disease peak and this
proliferation was augmented by exogenous IL-2. After prolonged cultur
e, proliferative response of CNS MNC to anti-CD3 mAb was restored. The
se results indicate that during monophasic EAE global suppression of n
aive T cell and Th1 T cell cytokine synthesis occurs but that T cell p
roliferative responsiveness is selectively inhibited in the CNS. (C) 1
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