| First Author | Liblau R | Year | 1997 |
| Journal | Int Immunol | Volume | 9 |
| Issue | 5 | Pages | 799-803 |
| PubMed ID | 9184926 | Mgi Jnum | J:40957 |
| Mgi Id | MGI:892676 | Doi | 10.1093/intimm/9.5.799 |
| Citation | Liblau R, et al. (1997) Experimental autoimmune encephalomyelitis in IL-4-deficient mice. Int Immunol 9(5):799-803 |
| abstractText | 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. |
