Th2 cells support intrinsic anti-inflammatory properties of the brain

J Neuroimmunol. 2001 Sep 3;119(1):73-80. doi: 10.1016/s0165-5728(01)00343-5.


In experimental autoimmune encephalomyelitis (EAE), Th1 cells are responsible for disease induction while Th2 cells can be protective. To address the mechanisms of this differential behavior, we utilized organotypic murine entorhinal-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 intercellular adhesion molecule-1 (ICAM-1) expression on microglia. Moreover, Th2 cells prevented or even reversed Th1-induced ICAM-1 upregulation. Evidently, Th2 cells could diminish Th1-induced inflammatory reactions and actively support the resting state of microglia, which could be one mechanism of Th2-mediated remission of neuroinflammation during EAE.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Brain / cytology
  • CD40 Antigens / metabolism
  • Cell Communication
  • Cell Movement / physiology
  • Cytokines / biosynthesis
  • Encephalitis / prevention & control*
  • In Vitro Techniques
  • Intercellular Adhesion Molecule-1 / metabolism
  • Mice
  • Mice, Inbred Strains
  • Microglia / metabolism
  • Microglia / physiology
  • Th1 Cells / physiology
  • Th2 Cells / physiology*


  • CD40 Antigens
  • Cytokines
  • Intercellular Adhesion Molecule-1