EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS IN IL-4-DEFICIENT MICE

Experimental autoimmune encephalomyelitis (EAE) is an inflammatory dem yelinating disease which usually follows a monophasic course, Autoreac tive T(h)1 CD4(+) T cells are responsible for the lesions, whereas aut oreactive T(h)2 CD4(+) T cells can, upon adoptive transfer, suppress t he disease process. However, the role of IL-4 and T(h)2 cells in the s pontaneous remission of EAE and in the prevention of relapses is not k nown, We have addressed these issues using IL-4-deficient mice in whic h the differentiation of T(h)2 CD4(+) T cells is severely compromised, The clinical course of actively induced EAE was compared in IL-4+/+, IL-4+/- and IL-4-/- mice on the PL/J genetic background. No significan t differences were noted between groups for the frequency, severity an d duration of EAE, and the frequency of relapses, Our results indicate that IL-4, despite its well-documented regulatory role in EAE, is not necessary for the spontaneous remission of disease or for the prevent ion of relapses, Therefore, in the absence of IL-4, overlapping or com pensatory immunoregulatory mechanisms can restrict an inflammatory res ponse within the central nervous system.