Acute autoimmune encephalomyelitis in mice. II. Susceptibility is controlled by the combination of H-2 and histamine sensitization genes

D. S. Linthicum, Jeffrey A Frelinger

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Abstract

The expression of acute experimental autoimmune encephalomyelitis (EAE) in mice is controlled by several dominant genes, H-2 and histamine sensitization genes. SJL/J and SWR/J, which are H-2(s) and H-2(q), respectively, are susceptible to EAE and sensitive to Bordetella pertussis histamine-sensitizing factor (HSF), which produces a vasoactive amine hypersensitivity. Other H-2(s) or H-2(q) strains such as A.SW, B10.Q and several others do not develop acute EAE and are not sensitive to B. pertussis HSF. One strain tested, DDD (K(s)I(s)D(?)) is HSF sensitive but does not develop EAE (presumably because it lacks the appropriate H-2 haplotype). However, F1 hybrids between B10.S and DDD are sensitive to HSF and develop EAE. The induction and effector phases of acute EAE are apparently controlled by the combination of H-2 and HSF genes. A combination of the correct H-2 haplotype and histamine sensitivity is required for the development of acute EAE.

Original languageEnglish (US)
Pages (from-to)31-40
Number of pages10
JournalJournal of Experimental Medicine
Volume156
Issue number1
StatePublished - 1982
Externally publishedYes

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Encephalomyelitis
Autoimmune Experimental Encephalomyelitis
Histamine
Pertussis Toxin
Genes
Dichlorodiphenyldichloroethane
Bordetella pertussis
Haplotypes
Dominant Genes
Amines
Hypersensitivity

ASJC Scopus subject areas

  • Immunology

Cite this

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title = "Acute autoimmune encephalomyelitis in mice. II. Susceptibility is controlled by the combination of H-2 and histamine sensitization genes",
abstract = "The expression of acute experimental autoimmune encephalomyelitis (EAE) in mice is controlled by several dominant genes, H-2 and histamine sensitization genes. SJL/J and SWR/J, which are H-2(s) and H-2(q), respectively, are susceptible to EAE and sensitive to Bordetella pertussis histamine-sensitizing factor (HSF), which produces a vasoactive amine hypersensitivity. Other H-2(s) or H-2(q) strains such as A.SW, B10.Q and several others do not develop acute EAE and are not sensitive to B. pertussis HSF. One strain tested, DDD (K(s)I(s)D(?)) is HSF sensitive but does not develop EAE (presumably because it lacks the appropriate H-2 haplotype). However, F1 hybrids between B10.S and DDD are sensitive to HSF and develop EAE. The induction and effector phases of acute EAE are apparently controlled by the combination of H-2 and HSF genes. A combination of the correct H-2 haplotype and histamine sensitivity is required for the development of acute EAE.",
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N2 - The expression of acute experimental autoimmune encephalomyelitis (EAE) in mice is controlled by several dominant genes, H-2 and histamine sensitization genes. SJL/J and SWR/J, which are H-2(s) and H-2(q), respectively, are susceptible to EAE and sensitive to Bordetella pertussis histamine-sensitizing factor (HSF), which produces a vasoactive amine hypersensitivity. Other H-2(s) or H-2(q) strains such as A.SW, B10.Q and several others do not develop acute EAE and are not sensitive to B. pertussis HSF. One strain tested, DDD (K(s)I(s)D(?)) is HSF sensitive but does not develop EAE (presumably because it lacks the appropriate H-2 haplotype). However, F1 hybrids between B10.S and DDD are sensitive to HSF and develop EAE. The induction and effector phases of acute EAE are apparently controlled by the combination of H-2 and HSF genes. A combination of the correct H-2 haplotype and histamine sensitivity is required for the development of acute EAE.

AB - The expression of acute experimental autoimmune encephalomyelitis (EAE) in mice is controlled by several dominant genes, H-2 and histamine sensitization genes. SJL/J and SWR/J, which are H-2(s) and H-2(q), respectively, are susceptible to EAE and sensitive to Bordetella pertussis histamine-sensitizing factor (HSF), which produces a vasoactive amine hypersensitivity. Other H-2(s) or H-2(q) strains such as A.SW, B10.Q and several others do not develop acute EAE and are not sensitive to B. pertussis HSF. One strain tested, DDD (K(s)I(s)D(?)) is HSF sensitive but does not develop EAE (presumably because it lacks the appropriate H-2 haplotype). However, F1 hybrids between B10.S and DDD are sensitive to HSF and develop EAE. The induction and effector phases of acute EAE are apparently controlled by the combination of H-2 and HSF genes. A combination of the correct H-2 haplotype and histamine sensitivity is required for the development of acute EAE.

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