In experimental autoimmune encephalomyelitis (EAE), Th1 cells are responsib
le for disease induction while Th2 cells can be protective. To address the
mechanisms of this differential behavior, we utilized organotypic murine en
torhinal-hippocampal slice cultures to analyze interactions between myelin
basic protein-specific Th1 and Th2 cells with microglial cells. While both
Th1 and Th2 cells induced CD40 expression, only Th1 cells induced intercell
ular adhesion molecule-1 (ICAM-1) expression on microglia. Moreover, Th2 ce
lls prevented or even reversed Th1-induced ICAM-1 upregulation. Evidently,
Th2 cells could diminish Th1-induced inflammatory reactions and actively su
pport the resting state of microglia, which could be one mechanism of Th2-m
ediated remission of neuroinflammation during EAE. (C) 2001 Elsevier Scienc
e B.V. All rights reserved.