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 radio-labeled cells to the brain. In F1 (Balb/c x SJL/J) mice that developed EAE and received anti-IAs antibody there was a decreased homing of radiolabeled cells when compared to animals that received anti-IAd antibody. In addition, there was preferential expression of IAs antigen, over IAd antigen on capillary endothelium of the brain. The differential expression of IA antigens and the homing of radiolabeled cells in F1 (SJL x Balb/c) mice could in part explain the haplotype-specific suppression of disease following treatment with anti-IA antibodies.
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