Essential Chemical Requirements for Induction of Allergic Encephalomyelitis

Westall, Fred C.; Robinson, Arthur L.; Caccam, Juanita F.; Jackson, Jesse J.; Eylar, E.H.

doi:10.1038/229022a0

Cited by 189 publications

(36 citation statements)

References 24 publications

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“…These observations are compatible with the view that differences in frequency between patients and controls should not be overrated in the implication of MBPspecific T cells in the pathogenesis of MS (48). More importantly, and for the first time to our knowledge, we show that the MBP region (111-129), encompassing the encephalitogenic epitopes for guinea pig strain 13 (41,58,59) and Lou/M rats (60), is largely immunodominant in human HLA-DRB1*0401-positive individuals. MBP(111-129)-specific, mostly DRB1* 0401-restricted TCL were detectable with no exception, and contributed Ͼ 50% of all MBP-specific TCL in the majority (9/12) of subjects (Table II).…”

Section: Discussionsupporting

confidence: 76%

Immunodominance of a low-affinity major histocompatibility complex-binding myelin basic protein epitope (residues 111-129) in HLA-DR4 (B1*0401) subjects is associated with a restricted T cell receptor repertoire.

et al. 1997

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Section: Discussionsupporting

confidence: 76%

Immunodominance of a low-affinity major histocompatibility complex-binding myelin basic protein epitope (residues 111-129) in HLA-DR4 (B1*0401) subjects is associated with a restricted T cell receptor repertoire.

et al. 1997

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“…Therefore, substitutions can be made in the original immunogen without destroying its activity. For example, it can be easily estimated that 10,000 peptides would satisfy the encephalitogenic requirements for the tryptophan peptide, fswgaegqr, of myelin basic protein (43,44,47).…”

mentioning

confidence: 99%

Molecular Mimicry Revisited: Gut Bacteria and Multiple Sclerosis

Westall¹

2006

J Clin Microbiol

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Molecular mimicry is a possible explanation for autoimmune side effects of microorganism infections. Protein sequences from a particular microorganism are compared to known autoimmune immunogens. For diseases such as multiple sclerosis (MS), where the infectious agent is unknown, guesses to its identity are made. Mimics are assumed to be rare. This study takes a radically different approach. Reported sequences from all known human bacterial and viral agents were searched for autoimmune immunogen mimics. Three encephalitogenic peptides, whose autoimmune requirements have been studied extensively, were selected for comparison. Mimics were seen in a wide variety of organisms. For each immunogen, the mimics were found predominantly in nonpathogenic gut bacteria. Since the three immunogens used in this study are related to MS, it is suggested that a microorganism responsible for autoimmune activity in MS could be a normally occurring gut bacterium. This would explain many of the peculiar MS epidemiological data and why no infective agent has been identified for MS and supports recently found MS gut metabolism abnormalities.

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“…The actual structure of the immunogenic determinant of murine CaBP must resemble the human EAE peptide, but is not necessarily identical. The conformational requirements for this determinant could possibly be explored by testing a range of synthetic peptides for their activity in vitro with tumour-bearing mouse PC, as has been done in vivo for the EAEinducing determinant of MBP (Westall, et al, 1971;Hashim, 1978;Khanarian et al, 1979).…”

Section: Discussionmentioning

confidence: 99%

Cellular immunity to encephalitogenic peptide in tumour-bearing mice

Yong¹,

Halliday²

1982

Br J Cancer

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Summary.-Mice bearing a methylcholanthrene-induced tumour were tested for their cell-mediated reactivity to the experimental allergic encephalomyelitis (EAE) peptide of human myelin basic protein (MBP) in the leucocyte adherence inhibition (LAI) test. Tested over a range of peptide concentrations, peritoneal cells (PC) from tumour-bearing mice exhibited optimal adherence inhibition at 640 ng/ml; PC from normal and parasite-infected mice were unreactive. The EAE peptide also stimulated PC from tumour-bearing mice in the E-rosette augmentation (ERA) test and in the macrophage migration inhibition (MMI) test. MMI appeared to be the most sensitive assay, in that significant reaction at peptide concentrations well below those giving significant LAI and ERA. LAI reactivity to the peptide was detected 5 days after tumour transplantation, and continued to be detectable even with very large tumours. In vitro assays were confirmed by demonstration of EAE peptide recognition in vivo, in tumour-bearing and tumour-excised mice, using the delayedtype hypersensitivity reaction. The present experiments demonstrate an antigenic determinant in murine tumours, similar to the well-characterized EAE peptide of human MBP, and establish an animal model for study and characterization of common tumour-associated antigens.

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Essential Chemical Requirements for Induction of Allergic Encephalomyelitis

Cited by 189 publications

References 24 publications

Immunodominance of a low-affinity major histocompatibility complex-binding myelin basic protein epitope (residues 111-129) in HLA-DR4 (B1*0401) subjects is associated with a restricted T cell receptor repertoire.

Immunodominance of a low-affinity major histocompatibility complex-binding myelin basic protein epitope (residues 111-129) in HLA-DR4 (B1*0401) subjects is associated with a restricted T cell receptor repertoire.

Molecular Mimicry Revisited: Gut Bacteria and Multiple Sclerosis

Cellular immunity to encephalitogenic peptide in tumour-bearing mice

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