Key result
In mice immunized with pertussis toxin, the eae9 locus controls experimental allergic encephalomyelitis susceptibility and severity, overriding other genetic checkpoints seen without the toxin.
The eae9 locus controls the effects of PTX in EAE susceptibility and can override other genetic checkpoints in the pathogenesis of the disease.
Requires validation beyond PTX-EAE mouse models before human relevance; leaves open broader genetic checkpoint roles in autoimmunity.
Pertussis toxin (PTX) is a potent ancillary adjuvant used to elicit several different autoimmune diseases, including experimental allergic encephalomyelitis (EAE). To delineate the genetics of PTX effect in EAE, we mapped EAE-modifying (eae-m) loci in cohorts of backcross mice immunized with and without PTX. In this study, we analyzed the genetic basis of EAE susceptibility and severity and the intermediate phenotypes of mononuclear cell infiltration, suppuration, and demyelination. In animals immunized with PTX, one major locus, eae9, controls disease susceptibility and severity. Eae9 also regulates the extent of mononuclear cell infiltration of the spinal cord in male mice. Without PTX, five eae-m loci were noted, including three new loci in intervals on chromosomes 8 (eae14), 10 (eae17), and 18 (eae18). Taken together, these results suggest that eae9 controls the effects of PTX in EAE susceptibility, and is capable of overriding the other genetic checkpoints in the pathogenesis of this disease.
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Blankenhorn et al. (2000) studied Experimental allergic encephalomyelitis (EAE). Pertussis toxin (PTX) immunization vs. Immunization without PTX was evaluated on EAE susceptibility and severity, and intermediate phenotypes (mononuclear cell infiltration, suppuration, and demyelination). In mice immunized with pertussis toxin, the eae9 locus controls experimental allergic encephalomyelitis susceptibility and severity, overriding other genetic checkpoints seen without the toxin.
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