Peptides used in Experimental Encephalomyelitis Models
Encephalomyelitis (EAE), is a widely used animal model for studies of multiple sclerosis. EAE is induced by stimulating T-cell-mediated immunity to myelin antigens. Active induction of EAE is accomplished by immunization with myelin antigens emulsified in adjuvant. The most common EAE models currently studied use rats and mice. Mice are favored because of the abundance of transgenic and targeted gene-deletion models and the numerous antibodies and immunomodulatory reagents available in this species that can be used to dissect the pathogenic mechanisms in EAE.
Multiple sclerosis (MS) is an inflammatory, demyelinating disease of the central nervous system (CNS). Even thought all MS patients exhibit signs of neurological deficit, there is considerable variation in the clinical signs and disease course among individuals. The pathology in the CNS is very heterogeneous, suggesting that MS may be more accurately described as a syndrome arising from multiple pathogenic pathways, rather than a single disease entity. Mechanistic insights into the complex pathogenesis of MS have relied extensively on animal models of CNS demyelination. Although several different models of demyelinating disease in the CNS exist, the most commonly used animal model for MS is EAE. EAE is induced by stimulating an immune response directed against CNS antigens. The origin of the model dates back to 1925 with the discovery that rabbits immunized with human spinal cord homogenate exhibited spinal cord inflammation and paralysis (referred to as active induction). In the 1930s, Rivers et al. showed that EAE could be induced in primates using multiple injections of emulsions of normal rabbit brain tissue. Subsequently, Paterson demonstrated that transfer of lymph node cells from rats immunized with spinal cord homogenate into naïve animals also induced EAE (referred to as passive induction).
Both multiple sclerosis and EAE are considered to be Th1-mediated autoimmune diseases in which neuroantigen-reactive lymphocytes infiltrate the CNS, mediate the development of inflammatory lesions, and in some models, trigger the demyelination of axons leading to progressive paralysis. Elevated levels of IL-12 have been reported in humans with progressive multiple sclerosis. Increased frequencies of IL-12–secreting monocytes appear to correlate with active brain lesions detected by magnetic resonance imaging. IL-12 has been functionally implicated in the development of EAE by the observations that αIL-12 (αp70) blocks disease development in mice and IL-12 p40–/– mice are resistant to EAE induction.
Active Induction of EAE with PLP and MBP Protein or Peptide
Experimental autoimmune encephalomyelitis (EAE) can be induced in SJL mice by immunization with proteolipid protein (PLP), myelin basic protein (MBP), or peptides. Peptides used correspond to the immunodominant epitopes of MBP (MBP84-104), MOG
(MOG92-106), or PLP (PLP139-151 and PLP178-191). In C57BL/6 mice the disease can be induced by immunization with the peptide corresponding to the immunodominant epitope of MOG (MOG35-55).
SJL Mice Info: Inbr: F104 (J). Albino. Genet: c, p, rd. Origin: Swiss Webster outbred stock from three sources that were brought to The Jackson Laboratory between 1938 and 1943, and pen-bred until 1955, when sib-mating was started. Although the strain has been developed relatively recently, it has rapidly become widely used owing to the high incidence of reticulum cell sarcomas resembling Hodgkin's disease. General biological data on the strain have been reviewed by Crispens (1973). Carries the pink-eyed dilution gene, p, which is derived from Asian mice of the Mus musculus type (see also strains 129/J, P/J and FS/Ei) (Brilliant et al, 1994). Source 1 and 2.
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