Role of Heredity in Experimental Disseminated Encephalomyelitis in Mice

Lee, Johanna M.; Olitsky, Peter K.; Schneider, Howard A.; Zinder, Norton D.

doi:10.3181/00379727-85-20906

Cited by 17 publications

(6 citation statements)

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“…A genetic analysis of the difference in susceptibility to experimental acute disseminated encephalomylitis (ADE) existing between BSVS mice (100 per cent susceptible) and BRVR mice (100 per cent resistant) has been reported previously (13). This report suggested that the resistance of the BRVR mice was due to two equlpotent genetic factors either of which, in single dosage, by simple dominance, was sufficient to confer resistance.…”

Section: Preliminary Observations Of a Nutritional Effect On Susceptimentioning

confidence: 85%

“…Historically, the development of this particular phenomenology has proceeded from a recognition of the consequences of injection into hosts of homologous and heterologous brain material (1, 2), the properties of adjuvants in enhancing the pathological effects of such injections (3,4), the more precise chemical definition of the injected brain material incitant (5)(6)(7)(8), the efficacy of various modes of injection (9), the role of hypersensitivity (10,11), with enhancement by Hemophilus pertussis vaccine (12), and the recognition of the genetic control of host susceptibility with a consequent Mendelian analysis of resistant and susceptible mouse genotypes (11,13). During the course of the genetic analysis evidence appeared which suggested that still another facet of this expanding phenomenology was open to experimental attack; namely, the effect of host nutrition on the capacity to elicit the disorder.…”

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confidence: 99%

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Effect of Nutrition on the Production of Acute Disseminated Encephalomyelitis in Mice

Schneider

Lee

Olitsky

1957

The Journal of Experimental Medicine

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The susceptibility of homozygous BSVS mice to acute disseminated encephalomyelitis (ADE) has been found to be nutritionally dependent. On a laboratory stock regimen of commercial fox chow pellets, whole wheat bread, and milk this genotype is 100 per cent susceptible to the disease. On a "synthetic" diet, containing a minimal list of vitamins adequate for growth and maintenance, susceptibility was found to be reduced to 15 per cent. Supplementation of the "synthetic" diet with biotin, folic acid, and vitamin B12 restored susceptibility to a frequency of 70 per cent. Increasing the supplements tenfold had no further effect in restoring susceptibility frequencies to the 100 per cent level. In the restoration of susceptibility, folic acid and vitamin B12 were equally effective as single supplements and equivalent to the triple vitamin supplement. The effect of single biotin supplementation was less. An outbreak of fatal pasteurellosis among BSVS mice latently infected with Pasteurella and used in an ADE susceptibility test has been described. The fatal pasteurellosis has been ascribed to a constellation of determinants including (a) diet, (b) sex, (c) inoculation events, and (d) latent infection with Pasteurella. With males the susceptible sex it was possible to avert the fatal pasteurellosis and continue the nutritional experiments by using females exclusively.

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Section: Preliminary Observations Of a Nutritional Effect On Susceptimentioning

confidence: 85%

mentioning

confidence: 99%

Effect of Nutrition on the Production of Acute Disseminated Encephalomyelitis in Mice

Schneider

Lee

Olitsky

1957

The Journal of Experimental Medicine

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“…Strain differences in susceptibility to EAE are well known, and the genetic basis has been studied best in mice. 38 It was most interesting that the individuality of our strains was based not merely on overall degree of susceptibility to EAE, but extended to different requirements for pertussis pretreatment and different patterns of reactivity to particular types of antigens. Predisposition to a particular type and extent of inflammatory response to antigens, with emphasis on participation of lymphocytes, may be one of the links between the genetic constitution and the phenotypic expression of susceptibility to EAE, but it is clearly not the only one.…”

Section: Discussionmentioning

confidence: 99%

INDUCTION OF EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS IN RATS WITHOUT THE AID OF ADJUVANT^*

Levine

Wenk

1965

Annals of the New York Academy of Sciences

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“…These findings were later applied to induce EAE in guinea pigs [6], mice [7], rats [8], rabbits, and other species. In the early 1950s it was recognized that strain-specific differences in susceptibility to EAE existed in mice and genetic analyses of resistant and susceptible mouse genotypes were carried out for the first time [9,10], showing that susceptibility to EAE was an inherited trait. Later, the immunological basis of EAE was confirmed when it was shown that disease could be adoptively transferred with sensitized lymphoid cells [11,12] and that disease induction could be prevented by thymectomy at birth [13].…”

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confidence: 99%

Genetics of Experimental Autoimmune Encephalomyelitis

Encinas

Kuchroo²

1999

Genes and Genetics of Autoimmunity

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The genetic basis for susceptibility to experimental autoimmune encephalomyelitis (EAE) has been the subject of intense study for several decades. In spite of this long history, however, the effort has only yielded small hints and contradictory leads to which genes influence susceptibility to this autoimmune disease. EAE is a prototypical model of autoimmunity that differs from other autoimmune diseases since it is relatively easily induced and quickly diagnosed in a wide range of strains and species. It also typically shows what looks, at first glance, to be a simple autosomal dominant inheritance pattern, making it appear to be an ideal disease to be solved genetically. In reality, however, the underlying genetics of EAE are much more complex than they appear on the surface, and the disease itself has a complex pathology that is only just beginning to be understood. With the advent in the last few years of transgene and knockout technologies and progress on the mapping and sequencing of genomes, strides are finally being made that promise to make an understanding of the genetics of EAE susceptibility a realizable goal. EAE is well established as a model for the human disease multiple sclerosis (MS), with resemblance in both its clinical and pathological features. Unlike MS, however, which is a spontaneous disease of unknown etiology, EAE is induced by driving the immune system to attack the brain and spinal cord through an immunization with any of several well-described central nervous system (CNS) myelin proteins. The disease that ensues begins with an inflammatory reaction in the white matter of the brain and spinal cord, causing both edema and myelin damage. As the inflammation progresses, damage to the myelin, which normally forms an insulating sheath around axons, leads to a disruption in the transmission of nerve signals along the spinal cord. This disruption typically manifests outwardly as paralysis in the tail and limbs.

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Role of Heredity in Experimental Disseminated Encephalomyelitis in Mice

Cited by 17 publications

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Effect of Nutrition on the Production of Acute Disseminated Encephalomyelitis in Mice

Effect of Nutrition on the Production of Acute Disseminated Encephalomyelitis in Mice

INDUCTION OF EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS IN RATS WITHOUT THE AID OF ADJUVANT^*

Genetics of Experimental Autoimmune Encephalomyelitis

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Role of Heredity in Experimental Disseminated Encephalomyelitis in Mice

Cited by 17 publications

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Effect of Nutrition on the Production of Acute Disseminated Encephalomyelitis in Mice

Effect of Nutrition on the Production of Acute Disseminated Encephalomyelitis in Mice

INDUCTION OF EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS IN RATS WITHOUT THE AID OF ADJUVANT*

Genetics of Experimental Autoimmune Encephalomyelitis

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INDUCTION OF EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS IN RATS WITHOUT THE AID OF ADJUVANT^*