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Inbred Strains of Mice: ABH

ABH (formerly AB/H)

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. \par

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. \par

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. \par

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. \par

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. \par

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. \par

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. \par

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. \par

Smith R. M., Morgan A., and Wraith D. C. (1994) Anticlass-II MHC antibodies prevent and treat EAE without depletion. Immunol. 83, 1-8. \par

Updated 9 Apr. 1998
Michael FW Festing
MRC Toxicology Unit, Hodgkin Building,
University of Leicester, UK

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