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T-cell vaccination prevents EAE effector cell development but does not inhibit priming of MBP responsive cells
1VAMC, Portland, OR 97201, USA.
Cell recipients which have recovered from adoptively transferred Experimental Allergic Encephalomyelitis (EAE) mediated by encephalitogenic T-cell lines do not develop clinical disease following subsequent challenge with myelin basic protein (MBP) emulsified in CFA (MBP-CFA), a recipient response termed vaccination. The immune mechanism(s), which accounts for the vaccination-induced resistance response, is not known. We have used an adoptive transfer system to investigate the point(s) of control within the pathway of EAE effector cell development from MBP-specific naive precursors that prevents clinical disease in T-cell line vaccinated, MBP-CFA challenged Lewis rats. Although EAE effector cells do not develop in T-cell line vaccinated recipients, our data shows that MBP precursor cells are primed in T-cell line vaccinated MBP-CFA challenged animals, and these MBP-specific precursor cells can be stimulated in culture to the EAE effector cell level. MBP-memory cells also arise in T-cell line vaccinated MBP-CFA challenged donors, as demonstrated by the early and rapid onset of EAE in MBP-CFA challenged recipients of lymphnode cells from T-cell line vaccinated MBP-CFA challenged donors. We also found that it was possible to adoptively transfer resistance to MBP-CFA challenge using spleen cells from donors previously vaccinated with encephalitogenic T-cells. These results show that although EAE effector cells do not develop in T-cell line vaccinated animals, T-cell vaccination does not inhibit the initial MBP precursor cell response and does not prevent the development of MBP memory cells.
Cell recipients which have recovered from adoptively transferred Experimental Allergic Encephalomyelitis (EAE) mediated by encephalitogenic T-cell lines do not develop clinical disease following subsequent challenge with myelin basic protein (MBP) emulsified in CFA (MBP-CFA), a recipient response termed vaccination. The immune mechanism(s), which accounts for the vaccination-induced resistance response, is not known. We have used an adoptive transfer system to investigate the point(s) of control within the pathway of EAE effector cell development from MBP-specific naive precursors that prevents clinical disease in T-cell line vaccinated, MBP-CFA challenged Lewis rats. Although EAE effector cells do not develop in T-cell line vaccinated recipients, our data shows that MBP precursor cells are primed in T-cell line vaccinated MBP-CFA challenged animals, and these MBP-specific precursor cells can be stimulated in culture to the EAE effector cell level. MBP-memory cells also arise in T-cell line vaccinated MBP-CFA challenged donors, as demonstrated by the early and rapid onset of EAE in MBP-CFA challenged recipients of lymphnode cells from T-cell line vaccinated MBP-CFA challenged donors. We also found that it was possible to adoptively transfer resistance to MBP-CFA challenge using spleen cells from donors previously vaccinated with encephalitogenic T-cells. These results show that although EAE effector cells do not develop in T-cell line vaccinated animals, T-cell vaccination does not inhibit the initial MBP precursor cell response and does not prevent the development of MBP memory cells.