COMPLEMENT-FIXING ANTIBRAIN ANTIBODIES AND ALLERGIC ENCEPHALOMYELITIS. I. CHARACTERIZATION OF THE ANTIBODIES.
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Biomedical subjects
Publications and source records attributed to P Y PATERSON.
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Rats regularly develop evidence of allergic encephalomyelitis (AE) 2 to 3 weeks following sensitization to nervous tissue plus adjuvant. Independent of the severity of AE which occurs, gradual recovery is the rule and by the 6th to 9th week after sensitization rats appear clinically well and microscopic lesions of AE have virtually disappeared. Pooled serum collected from rats 3 or 6 weeks after sensitization contains complement-fixing (CF) antibrain antibodies. Such pooled serum exerts a striking suppressive influence on development of AE when passively administered to rats actively sensitized to nervous tissue. Serum pools which contain CF antibrain antibody suppress the disease. Serum pools lacking CF antibody do not suppress the disease. Serum containing CF antibrain antibody after treatment with 2-mercaptoethanol no longer fixes complement with brain antigen in vitro and no longer suppresses AE in vivo. The data suggest that transfer of protection against AE by passively administered antibrain rat serum is due to an antibrain antibody, possibly the CF antibodies. The meaning of these findings is discussed in terms of the role(s) of circulating antibrain antibody in the pathogenesis of AE.
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Rats, in contrast to certain other species of animals reported, have a striking capacity to develop allergic encephalomyelitis within 2 to 3 weeks following one injection of spinal cord antigen combined with Freund's incomplete adjuvant-that is, adjuvant prepared without addition of killed mycobacteria.
Transfer of allergic encephalomyelitis has been accomplished by injection of lymph node cells, obtained from donor rats sensitized to spinal cord, into recipient rats pretreated neonatally with normal rat spleen cells. Transfer of the disease may be achieved most frequently when the recipients are pretreated with spleen cells of the prospective lymph node cell donors. These transfers are attributed to the use of recipients which have acquired immunological tolerance to donor lymph node cells, as a result of the spleen cell pretreatment, and in which, therefore, the donor cells can survive and function longer after transfer.
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