Observations on Attempts to Produce Acute Disseminated Encephalomyelitis in Monkeys

Abstract

No evidence was found to support the idea that vaccine virus placed in the cisterna magna is capable of producing an acute disseminated encephalomyelitis with perivascular demyelination either in normal or in partially immune monkeys. A testicular extract (Reynals' factor) did not induce vaccine virus to cause an acute disseminated encephalomyelitis in monkeys. Repeated intramuscular injections of brain extracts and brain emulsions into eight monkeys were followed in two instances by an inflammatory reaction, accompanied by demyelination, in the central nervous system. The exact relation of the injections to the disease of the nervous system is not clear. The combined action of vaccine virus and an emulsion of fresh rabbit brain did not lead to the production of an acute disseminated encephalomyelitis in monkeys that had received repeated intramuscular injections of emulsions and alcohol-ether extracts of normal rabbit brains.

The gray aspects of white matter disease in multiple sclerosis

“…The discovery of EAE in 1933 was marked by its diamond anniversary in 2008 (12,13). Twenty-eight years ago researchers, including one of the senior authors of ref.…”

Effective Antigen-Specific Immunotherapy in the Marmoset Model of Multiple Sclerosis

“…The disease exhibits relapsing and remitting symptoms including disturbances in vision, speech, coordination, and cognition as well as weakness, spasticity, and paralysis (1,2). Lymphocytic infiltration in the CNS white matter and immune reactions against myelin Ags indicate an autoimmune etiology for MS (1)(2)(3)(4)(5)(6)(7)(8). Allergic encephalomyelitis was first observed as a side effect of the rabies vaccine prepared from rabbit brains by Pasteur in the 1880s (see Ref.…”

“…3). Rivers and others showed that the CNS inflammation was caused not by the rabies virus but by immune sensitization to the combination of adjuvant and brain tissue contaminating the vaccine (3,4). Experimental allergic encephalomyelitis (EAE) models in various animal species, typically rodents, were later developed by immunization with myelin proteins in adjuvant or by the adoptive transfer of myelinreactive T cells, causing inflammatory damage to the white matter (1)(2)(3)(4)(5)(6).…”

“…Encephalitogenic CD4 ϩ T cells are believed to initiate and perpetuate EAE and MS and thus constitute a therapeutic target (1)(2)(3)(4)(5)(6)(7)(8). Abundant myelin protein Ags, including myelin basic protein (MBP) and proteolipid protein (PLP) as well as the less abundant Ags, myelin oligodendrocyte glycoprotein (MOG) and myelin-associated glycoprotein (MAG), are recognized by T cells in MS patients (9 -11).…”

Multiple Sclerosis and Regulatory T Cells

“…These genetic risk factors manifest in autoimmune inflammation, Evidence of the inflammatory nature of MS dates back to 1948, when Elvin Kabat observed that MS patients have abnormally high levels of oligoclonal immunoglobulin in the cerebrospinal fluid (CSF) [4]. Self-antigen directed inflammation is thought to precede development of MS; this relationship has been demonstrated in experimental autoimmune encephalomyelitis (EAE), an animal model of MS [5]. In this animal model, the minimal requirement for inducing CNS inflammation is activation of myelin reactive T cells in the peripheral immune system [6].…”