To elucidate the involvement of interleukin-1βconverting enzyme (ICE) in the course of experimental autoimmune encephalomyelitis (EAE), we induced EAE by immunizing rats with an emulsion of rat spinal cord homogenate with complete Freund´s adjuvant supplemented with Mycobacterium tuberculosis (H37Ra, 5㎎/㎖) and then examined the expression of ICE in the spinal cord of rats with EAE.
In normal rat spinal cords, ICE is constitutively, but weakly, expressed in ependymal cells, neurons, and some neuroglial cells. In EAE, many inflammatory cells are positive for ICE, and the majority of ICE+ cells were identified as ED1+ macrophages. During this stage of EAE, the number of ICE+ cells in brain cells, including neurons and astrocytes, increased and these cells also had increased ICE immunoreactivity.
These findings suggest that the upregulation of ICE in both brain cells and invading hematogenous cells is stimulated by a secretory product from inflammatory cells, and that this enzyme is involved in the pathogenesis of EAE via the production of IL-1 beta.
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