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T Cells Enhance the Expression of Experimental Autoimmune Encephalomyelitis by Promoting Antigen Presentation and IL-12 Production1
* Department of Neurology, Medical University of Lodz, Lodz, Poland;
Department of Human Developmental Biology, Jagiellonian University College of Medicine, Cracow, Poland; and
Department of Pathology (Neuropathology), Albert Einstein College of Medicine, Bronx, NY 10461
Using an adoptive transfer model of experimental autoimmune encephalomyelitis (EAE) induced by myelin basic protein (MBP)-reactive lymph node cells (LNC), we have shown that depletion of 
T cells from LNC resulted in diminished severity of EAE in recipient mice, both clinically and histopathologically. The reduced potency of T cell-depleted LNC to induce EAE correlated with decreased cell proliferation in response to MBP. The T cell effect upon the threshold of MBP-induced LNC proliferation and EAE transfer was restored by reconstitution of T cells derived from either MBP-immunized or naive mice, indicating that this effect was not Ag specific. The enhancing effect of T cells on MBP-induced proliferation and EAE transfer required direct cell-to-cell contact with LNC. The T cell effect upon the LNC response to MBP did not involve a change in expression of the costimulatory molecules CD28, CD40L, and CTLA-4 on TCR
+ cells, and CD40, CD80, and CD86 on CD19+ and CD11b+ cells. However, depletion of T cells resulted in significant reduction in IL-12 production by LNC. That T cells enhanced the MBP response and severity of adoptive EAE by stimulating IL-12 production was supported by experiments showing that reconstitution of the T cell population restored IL-12 production, and that T cell depletion-induced effects were reversed by the addition of IL-12. These results suggest a role for T cells in the early effector phase of the immune response in EAE.
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