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-2s and H-2q, respectively, are susceptible to EAE and sensitive to Bordetella pertussis histamine-sensitizing factor (HSF), which produces a vasoactive amine hypersensitivity. Other H-2s or H-2q 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 (KsIsD?) is HSF sensitive but does not develop EAE (presumably because it lacks the appropriate responder 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 hapotype and histamine sensitivity is required for the development of acute EAE.
MeSH Terms
Acute Disease
Adjuvants, Immunologic/pharmacology
Animals
Encephalomyelitis, Autoimmune, Experimental/genetics,immunology
Female
Genes, MHC Class II
H-2 Antigens/genetics,immunology
Histamine/genetics,immunology
Male
Mice
Mice, Inbred BALB C
Mice, Inbred C57BL
Mice, Inbred CBA
Mice, Inbred DBA
Mice, Inbred NZB
Pertussis Toxin
Recombination, Genetic
Virulence Factors, Bordetella
Chemicals
Adjuvants, Immunologic
H-2 Antigens
Virulence Factors, Bordetella
Histamine
Pertussis Toxin
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Linthicum D S
Frelinger J A
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