Induction of resistance to active experimental allergic encephalomyelitis by myelin basic protein‐specific Th2 cell lines generated in the presence of glucocorticoids …

F Ramírez, D Mason - European Journal of Immunology, 2000 - Wiley Online Library
F Ramírez, D Mason
European Journal of Immunology, 2000Wiley Online Library
We have produced T cell lines with a Th2 phenotype in the presence of IL‐4 and the
glucocorticoid dexamethasone (DEX). IL‐4 and DEX together were more effective in
inducing a Th2 response than IL‐4 alone. Myelin basic protein (MBP)‐specific Th2 lines
were obtained and their ability to induce experimental allergic encephalomyelitis (EAE) was
studied. Lines treated with IL‐4 and DEX did not transfer passive EAE and did not induce
cellular infiltration into the central nervous system as opposed to the encephalitogenic Th1 …
Abstract
We have produced T cell lines with a Th2 phenotype in the presence of IL‐4 and the glucocorticoid dexamethasone (DEX). IL‐4 and DEX together were more effective in inducing a Th2 response than IL‐4 alone. Myelin basic protein (MBP)‐specific Th2 lines were obtained and their ability to induce experimental allergic encephalomyelitis (EAE) was studied. Lines treated with IL‐4 and DEX did not transfer passive EAE and did not induce cellular infiltration into the central nervous system as opposed to the encephalitogenic Th1 lines. Lines treated with IL‐4 and DEX did not protect animals from the effect of encephalitogenic Th1 lines when the two were injected together. However, a high proportion of animals injected with IL‐4 + DEX‐treated lines became refractory to the development of EAE after immunization with MBP; that is, it was possible to induce resistance to active EAE without prior episodes of disease. Interestingly, animals injected with T cell lines had accelerated antibody responses against MBP and the predominant isotype was dependent on the cytokines synthesized by the T cell line injected. There was not evidence that the resistance to active EAE was due to anergy of MBP‐reactive cells or the action of CD8+ cells. Our data suggest that MBP‐specific T cell lines prevent the induction of disease by deviating the reactivity to MBP from a cellmediated to a humoral one and not merely from a Th1 to a Th2 response.
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