TY - JOUR
T1 - EXPERIMENTAL AUTOIMMUNE ENCEPHALO‐MYELITIS IN MICE
T2 - GENETIC CONTROL OF SUSCEPTIBILITY
AU - Bernard, C. C A
PY - 1976
Y1 - 1976
N2 - Experimental autoimmune encephalomyelitis (EAE) was induced in inbred and congenic strains of mice by injection of mouse spinal cord homogenate (MSCH) in Freund's complete adjuvant (FCA) with pertussis vaccine. Genetic analyses showed that susceptibility to EAE in mice was inherited as a dominant trait and was in part controlled by genes located in the centromeric half of the H‐2 complex. Mice with EAE developed cell‐mediated immune responsiveness to basic protein of myelin (BPM), as judged by the macrophage migration inhibition assay, using peritoneal exudate cells; this was not observed with mice of resistant strains. However, the migration of peritoneal exudate cells of both susceptible and resistant strains was significantly inhibited in the presence of purified protein derivative (PPD) of M. tuberculosis. Thus, the genes involved in the control of susceptibility to EAE also influence T cell responsiveness to BPM. Antibody to BPM, as judged by radioimmunoassay, was detected in susceptible and resistant strains but there was no correlation between the presence or levels of antibody and susceptibility or resistance to EAE. It is suggested that resistance to EAE is associated with failure of T cells to recognize and/or respond to the encephalitogenic determinant of the BPM molecule.
AB - Experimental autoimmune encephalomyelitis (EAE) was induced in inbred and congenic strains of mice by injection of mouse spinal cord homogenate (MSCH) in Freund's complete adjuvant (FCA) with pertussis vaccine. Genetic analyses showed that susceptibility to EAE in mice was inherited as a dominant trait and was in part controlled by genes located in the centromeric half of the H‐2 complex. Mice with EAE developed cell‐mediated immune responsiveness to basic protein of myelin (BPM), as judged by the macrophage migration inhibition assay, using peritoneal exudate cells; this was not observed with mice of resistant strains. However, the migration of peritoneal exudate cells of both susceptible and resistant strains was significantly inhibited in the presence of purified protein derivative (PPD) of M. tuberculosis. Thus, the genes involved in the control of susceptibility to EAE also influence T cell responsiveness to BPM. Antibody to BPM, as judged by radioimmunoassay, was detected in susceptible and resistant strains but there was no correlation between the presence or levels of antibody and susceptibility or resistance to EAE. It is suggested that resistance to EAE is associated with failure of T cells to recognize and/or respond to the encephalitogenic determinant of the BPM molecule.
UR - http://www.scopus.com/inward/record.url?scp=0017167922&partnerID=8YFLogxK
U2 - 10.1111/j.1744-313X.1976.tb00583.x
DO - 10.1111/j.1744-313X.1976.tb00583.x
M3 - Article
C2 - 1109134
AN - SCOPUS:0017167922
VL - 3
SP - 263
EP - 274
JO - International Journal of Immunogenetics
JF - International Journal of Immunogenetics
SN - 1744-3121
IS - 4
ER -