Inbred Strains
of Mice: ABH
Inbr. F46 (Dr. David Baker, Jan. 1995). Albino. Genet.
Thy1a,
Ly1b, Ly2b,
Ly5b ,
H2dq1
(Fairchild et al 1993). Origin: Inbred (
Baker
et al 1990) from outbred mice selected by Biozzi for high antibody
response to sheep red blood cells (Feingold et al 1976). Note that other
strains originating from the same outbred selected stock may differ from
ABH. Susceptible to the development of experimental allergic encephalomyelitis
(EAE) following injection of spinal cord homogenate in adjuvant. The mice
develop a chronic relapsing pattern of disease characterised by mononuclear
infiltration of the central nervous system, with demyelination being particularly
evident in relapse. Treatment with sciatic nerve homogenate results in
experimental allergic neuritis (
O'Neill
et al 1992). These mice appear to be a good model of multiple sclerosis
(
Baker et al 1990). The T-cell receptor
has a deletion ligand encoded by MTV7 (Fairchild et al 1993). A major
encephalitogenic epitope of a protolipid protein has been identified (
Amor et al 1993, 1994). Immune response genes
characterised by Liu et al (
1993). The MHC
antibody OX6 is able to prevent and treat EAE in these mice (
Smith et al 1994), and CD4-depleating or CD4 blocking monoclonal
antibody significantly inhibited disease progression (
O'Neill et al 1993). The experimental encephalomyelitis
modulates inositol and taurine in the spinal cord (
Preece et al, 1994). The protease inhibitor D-penicillamine
attenuated the exacerbations even when treatment was started after the
primary full-blown disease had developed (
Norga
et al, 1995).
In crosses with NOD there was evidence of genetic linkage between the
experimental allergic encephalomyelitis and genes on ten chromosomes,
with particularly strong linkage to chromosomes 7, 11 and 18 (Baker et al, 1995).
Amor S., Baker
D., Groome N., and Turk J. L. (1993) Identification of a major encephalitogenic
epitope of proteolipid protein (residues-56-70) for the induction of experimental
allergic encephalomyelitis in Biozzi AB/H and Non-obese diabetic mice.
J. Immunol. 150, 5666-5672.
Baker D.,
O'Neil J. K., Gschmeissner S. E., Wilcox C. E., Butter C., and Turk J.
L. (1990) Induction of chronic relapsing experimental allergic encephalomyelitis
in Biozzi mice. J. Neuroimmunol. 28, 261-270.
Baker D.,
Rosenwasser O. A., O'Neill J. K., and Turk J. L. (1995) Genetic analysis
of experimental allergic encephalomyelitis in mice. J. Immunol.
155, 4046-4051.
Liu G. Y., Baker
D., Fairchild S., Figueroa F., Quartey-Papafio R., Tone M., Healey D.,
Cooke A., Turk J. L., and Wraith D. C. (1993) Complete characterization
of the expressed immune response genes in Biozzi AB/H mice: structural
and functional identity between AB/H and NOD A region molecules. Immunogenet.
37, 296-300.
Norga K.,
Paemen L., Masure S., Dillen C., Heremans H., Billiau A., Carton H., Cuzner
L., Olsson T., Van Damm J., and Opdenakker G. (1995) Prevention of acute
autoimmune encephalomyelitis and abrogation of relapses in murine models
of multiple sclerosis by the protease inhibitor D-penicillamine. Inflam.
Res. 44, 529-534.
O'Neill
J. K., Baker D., and Turk J. L. (1992) Inhibition of chronic relapsing
experimental allergic encephalomyelitis in the Biozzi AB/H mouse. J.
Neuroimmunol. 41, 177-187.
O'Neill
J. K., Baker D., Davison A. N., Allen S. J., Butter C., and Waldmann H.
(1993) Control of immune-mediated disease of the central-nervous-system
with monoclonal (CD4-specific) antibodies. J. Neuroimmunol. 45,
1-14.
Preece
N. E., Amor S., Baker D., Gadian D. G., O'Neill J. K., and Urenjak J.
(1994) Experimental encephalomyelitis modulates inositol and taurine in
the spinal cord of biozzi mice. Magnetic Resonance in Medicine
32, 692-697.
Smith R.
M., Morgan A., and Wraith D. C. (1994) Anticlass-II MHC antibodies prevent
and treat EAE without depletion. Immunol. 83, 1-8.
INBRED STRAINS OF MICE
Updated 9 Apr. 1998
Michael FW
Festing
MRC Toxicology Unit, Hodgkin Building,
University of Leicester,
UK
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