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

Abstract

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 demonstrates 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.