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The Journal of Immunology, Vol 140, Issue 11 3701-3706, Copyright © 1988 by American Association of Immunologists
ARTICLES |
ME Kanof and SP James
Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892.
Previous studies have suggested that there is an inverse relationship between cell activation and the expression of the Leu-8 Ag, a cell surface protein that distinguishes functionally distinct T cell populations. This was confirmed in vitro, because when resting PBL were activated with PHA there was a rapid decline in expression of the Leu-8 Ag on all lymphocyte subpopulations. A decline in Leu-8 reactivity occurred after stimulation of lymphocytes with PHA, anti-CD3 plus PMA and ionomycin plus PMA, and an intermediate decline in Leu-8 expression occurred after stimulation with Con A. However, there was little loss of expression of Leu-8 after stimulation of lymphocytes with PWM or allogeneic lymphocytes. The decline in Leu-8 expression on activated lymphocytes occurred earlier than the decline in expression of CD45R. After removal of the activation stimuli, peripheral blood T cells or Jurkat cells rapidly re-expressed Leu-8. Finally, when the expression of Leu-8 on peripheral blood CD4+, Leu-8+ T cells was reduced by prior activation with PHA, these cells continued to exhibit suppressor function for PWM-stimulated Ig synthesis. Thus, there is a rapid decline in expression of the Leu-8 Ag but no change in regulatory function of CD4+, Leu-8+ T cells during cell activation. These results suggest that the molecule recognized by anti-Leu-8 plays a role in lymphocyte activation but not directly in the effector function of CD4+, Leu8+ T cells.
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