Abstract
In vivo treatment with anti-IA antibodies has been shown to induce a haplotype-specific inhibition of EAE when the disease was following passive transfer of MBP-sensitized T cells. In order to determine the mechanism by which anti-IA antibody prevents passively transferred EAE, the homing of radiolabeled cells to the brain following anti-IA therapy was studied. Administration of anti-IA antibodies at the earliest onset of clinical signs of EAE prevented the homing of radiolabeled cells to the brain. In Fl (Balb/c X SJL/J) mice that developed EAE and received anti-IA s antibody there was a decreased homing of radiolabeled cells when compared to animals that received anti-IA d antibody. In addition, there was preferential expression of IA s antigen, over IA d antigen on capillary endothelium of the brain. The differential expression of IA antigens and the homing of radiolabeled cells in Fl (SJL X Balb/c) mice could in part explain the haplotypespecific suppression of disease following treatment with anti-IA antibodies.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
