Table 15.1.1.
Mouse strain | H-2 type | Peptide | Sequencea | Reference |
---|---|---|---|---|
PL/J, B10.PL | H-2u | MBPAc1-11 | Ac-ASQKRPQRHG | Zamvil et al. (1986) |
PLP178-191 | NTWTTCQSIAFPSK | Unpublished (B10.PL) | ||
MBP35-47 | TGILDSIGRFFSG | Zamvil et al. (1988) | ||
PLP43-64 | EKLIETYFSKNYQDYEYLINVI | Whitham et al. (1991) | ||
SJL | H-2s | MBP89-101 | VHFFKNIVTPRTP | Sakai et al. (1988) |
MBP84-104 | VHFFKNIVTPRTPPPSQGKGR | Tan et al. (1992) | ||
PLP139-151b | HSLGKWLGHPDKF | Tuohy et al. (1993) | ||
PLP104-117 | KTTICGKGLSATVT | Tuohy and Thomas (1993) | ||
PLP178-191 | NTWTTCQSIAFPSK | Greer et al. (1992) | ||
PLP57-70 | YEYLINVIHAFQYV | Greer et al. (1996) | ||
MOG92-106 | DEGGYTCFFRDHSYQ | Amor et al. (1994) | ||
(PL/J X SJL) F1 | H-2s/u | MBPAc1-11 | Ac-ASQKRPQRHG | Zamvil et al. (1986) |
PLP43-64 | EKLIETYFSKNYQDYEYLINVI | Whitham et al. (1991) | ||
PLP139-151 | HSLGKWLGHPDKF | Whitham et al. (1991) | ||
C57BL/6 | H-2b | MOG35-55 | MEVGWYRSPFSRVVHLYRNGK | Mendel et al. (1995) |
PLP178-191 | NTWTTCQSIAFPSK | Tompkins et al. (2002) | ||
C3H | H-2k | PLP103-116 | YKTTICGKGLSATV | Tuohy et al. (1988a) |
SWR | H-2q | PLP215-232 | PGKVCGSNLLSICKTAEF | Endoh et al. (1990) |
(SJL X B10.PL) F1 | H-2s/q | PLP139-151 | HSLGKWLGHPDKF | Unpublished |
PLP178-191 | NTWTTCQSIAFPSK | Unpublished | ||
MBPAc1-11 | Ac-ASQKRPQRHG | Unpublished | ||
(SJLX C3H/HeJ)F1c | H-2s/k | PLP190-209 | SKTSASIGSLCADARMYGVL | Muller et al. (2000) |
PLP215-232 | PGKVCGSNLLSICKTAEFQ | Greer et al. (1996) | ||
BALB/cPtc | H-2d | PLP178-191 | NTWTTCQSIAFPSK | Greer et al. (1992) |
NOD | H-2g7 | PLP56-70 | DYEYLINVIHAFQYV | Girvin et al. (2000) |
MOG35-55 | MEVGWYRSPFSRVVHLYRNGK | Slavin et al. (1998) |
Sequences for MBP peptides are based on different species variants of MBP, which have different numbering systems; sequences for PLP and MOG peptides are based on the mouse sequence. The reader is urged to consult the indicated references for more detailed information.
The PLP139-151 sequence has a serine (S) for cysteine (C) substitution at position 140 to enhance solubility.
The EAE observed in these mice is nonclassical. In (SJL X C3H/HeJ)F1 mice, the disease causes imbalance and axial rotary movement (rotary EAE). In BALB/cPt, mice show lack of balance and forelimb paralysis in the absence of hindlimb paralysis.