Experimental allergic encephalomyelitis (EAE) in mice lacking CD4+ T cells

Eur J Immunol. 1994 Sep;24(9):2250-3. doi: 10.1002/eji.1830240947.


Like most experimental autoimmune disease experimental allergic encephalomyelitis (EAE) has been shown to be mediated by CD4+ helper T cells. In vivo antibody blocking studies with anti-CD4 and adoptive transfer of activated CD4+ T cells indicate the importance of CD4+ cells in disease induction. Fourth backcross generation mutant CD4-/-PL/J mice were immunized with myelin basic protein. Despite the lack CD4+ T cells some of these mice developed EAE, albeit, at a considerably reduced frequency and with variable severity. Furthermore, antigen-specific T cell proliferation can be demonstrated, indicating some residual helper activity that is major histocompatibility complex class II restricted. This demonstrated that, although the CD4+ T cell is the prime effector cell in EAE, in mice developmentally lacking in CD4, the expanded double-negative T cells may subserve helper and effector functions.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antibodies, Monoclonal
  • CD4-Positive T-Lymphocytes / immunology*
  • Encephalomyelitis, Autoimmune, Experimental / immunology*
  • Interleukin-2 / immunology
  • Lymphocyte Activation / immunology
  • Mice
  • Mice, Mutant Strains


  • Antibodies, Monoclonal
  • Interleukin-2