The role of macrophages in different stages of experimental allergic encephalomyelitis in Lewis rats

Abstract

Experimental allergic encephalomyelitis (EAE) is a T cell mediated inflammatory disease of the central nervous system (CNS) which results in neurologic disorders such as paralysis of the hind limbs and bladder dysfunction. EAE can be induced in susceptible animals by immunization with encephalitogenic proteins present in homogenates of neural tissues (1). In particular the chronic relapsing form (CREAE), which can be induced by treatment with low doses of cyclosporin A (2), resembles in many aspects the human disease multiple sclerosis. The clinical course of CREAE, with its relapses and remissions, is very similar to that of multiple sclerosis (2), as are the pathological findings in the CNS. In both multiple sclerosis (3) and CREAE (2) perivascular infiltrates occur in the CNS consisting of macrophages and T lymphocytes, accompanied by an increased expression of MHC class II antigens on a variety of cells. Pronounced demyelination, one of the characteristic pathological features of multiple sclerosis, has also been described in the cyclosporin-induced CREAE (5). CREAE is thus a useful animal model for multiple sclerosis, in particular when the effector phase is studied, rather than aetiological factors.