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The Journal of Immunology, Vol 155, Issue 4 1873-1883, Copyright © 1995 by American Association of Immunologists
ARTICLES |
TL Walunas, DS Bruce, L Dustin, DY Loh and JA Bluestone
Committee on Immunology, University of Chicago, IL 60637, USA.
This study examined long-term phenotypic and functional effects of TCR ligation in vivo. Flow cytometric analysis of T cells from mice treated with anti-CD3 revealed an increase in CD44 expression in both the CD4+ and CD8+ populations. The phenotypic changes were a result of TCR engagement, because treatment with staphylococcal enterotoxin B (SEB) resulted in a preferential increase in CD44 expression on the SEB- reactive V beta 8 T cells. In addition, the percentage of cells expressing Ly-6C increased among the CD8+ subset after anti-CD3 treatment and in the V beta 8+ CD8+ subset after treatment with SEB. Finally, the TCR transgenic (Tg) mouse strain 2C was used to confirm that the phenotypic changes can be induced by exposure to a physiologic ligand (H-2Ld). Before treatment, nearly all of the Tg+CD8+ cells were CD44low/Ly-6C-. Tg+ peritoneal exudate T cells isolated from mice challenged with P815 cells (H-2Ld) up-regulated Ly-6C and secreted higher levels of IFN-gamma on a per Tg+ CD8+ T cell basis after treatment. Taken together, these data indicate that in vivo TCR/CD3 engagement results in phenotypic and functional changes in T cells. Furthermore, Ly-6C expression correlates with an increase in IFN-gamma production after antigenic stimulation of CD8+ T cells, suggesting that it is a "memory" marker that correlates with Ag-specific functional changes in CD8+ T cells.
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