Table 15.1.6.

Mouse TCR Transgenic Models of EAE

Background (MHC restriction)	TCR Specificity	Characterization of disease parameters	Reference
19G B10.PL (I-Au)	Mouse MBPAc1-11	High spontaneous incidence (100%) of conventional EAE on RAG-1−/− background with onset at ∼7-8 weeks; low incidence (∼15%) on conventional B10.PL background	Lafaille et al. (1994)
5B6 SJL (I-As)	Mouse PLP139-151	Moderate spontaneous incidence (40%-60%) on conventional SJL background; more severe conventional EAE upon peptide immunization and/or treatment with pertussis toxin	Waldner et al. (2000)
2D2 C57BL/6 (H-2b)	Mouse MOG35-55	No spontaneous conventional EAE, but ∼30% incidence of spontaneous optic neuritis; more severe induction of conventional EAE upon peptide immunization and/or treatment with pertussis toxin	Bettelli et al. (2003)
(2D2 × IgHMOG)F1	Mouse MOG35-55	60% incidence of spontaneous conventional EAE in F1 mice with demyelinating lesions restricted to optic nerve and spinal cord, sparring the cerebellum	Madsen et al. (1999); Ellmerich et al. (2005)
HLA-DR2 (DRA*0101/DRB1*1501)	Human MBP84-102 (Ob1.A12)	Only ∼4% spontaneous EAE in (HLA-DR2 × Ob1.A12) F1 mice; high disease incidence (∼85% to 90%) in F1 mice primed with peptide and treated with pertussis toxin with variable clinical symptoms	Madsen et al. (1999)
HLA-DR15	Human MBP84-102 (Ob1.A12)	Line 7 transgenics develop spontaneous paralyses at 4 to 5 months of age at a level of 60% (wild-type background) and 100% (Rag-1−/− background) and responses spread to other DR15-restricted myelin epitopes; other lines develop disease only upon peptide priming and treatment with pertussis toxin	Ellmerich et al. (2004, 2005)
DRB1*0401	Human MBP111-129 (MS2-3C8)	Disease incidence in HLA-DRB1*0401 transgenic recipients of transgenic T cells ranged from 60% to 100%; clinical signs consist of ascending hindlimb paralysis along with atypical signs consistent with demyelination within the brainstem and cranial nerve roots	Quandt et al. (2004)