Unlike Lewis strain, BN rats do not develop EAE when given 10 microgram GPBP + CFA. Their resistance is mediated via the MHC-linked gene Ir-EAE-. The cellular mechanism of BN resistance can be probed using bone marrow chimeras between susceptible LBNF1 strain and BN. F1 leads to BN chimeras can develop EAE when actively sensitized with GPBP + CFA, but are markedly more resistant than F1 leads to F1. By contrast, F1 leads to BN chimeras are highly susceptible to passively transferred EAE from an F1 donor. F1 rats reconstituted with BN bone marrow, i.e., BN leads to F1 chimeras, are completely resistant to EAE induced by active sensitization, but they too are susceptible to passively transferred EAE. We argue that Ir-EAE- blocks the development of T cells reactive to self myelin, and that this occurs at the level of macrophage presentation of antigen to the T cell. Suppressor mechanisms do not appear to play a major role.

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