Experimental autoimmune encephalomyelitis in IL-4-deficient mice.
Experimental autoimmune encephalomyelitis (EAE) in an inflammatory demyelinating disease which usually follows a monophasic course. Autoreactive Th1 CD4+ T cells are responsible for the lesions, whereas autoreactive Th2 CD4+ T cells can, upon adoptive transfer, suppress the disease process. However, the role of IL-4 and Th2 cells in the spontaneous remission of EAE and in the prevention of relapses is not known. We have addressed these issues using IL-4-deficient mice in which the differentiation of Th2 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 significant differences were noted between groups for the frequency, severity and 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 prevention of relapses. Therefore, in the absence of IL-4, overlapping or compensatory immunoregulatory mechanisms can restrict an inflammatory response within the central nervous system.
Liblau
R
R
Department of Microbiology and Immunology, Stanford University School of Medicine, CA 94305, USA.
Steinman
L
L
Brocke
S
S
D000818:Animals; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000209:etiology / Q000235:genetics* / Q000276:immunology*; D015847:Interleukin-4 / Q000172:deficiency* / Q000235:genetics* / Q000276:immunology; D051379:Mice; D008817:Mice, Mutant Strains; D012008:Recurrence; D012075:Remission, Spontaneous; D018418:Th2 Cells / Q000276:immunology
D015847:Interleukin-4