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From the * Department of Microbiology and Immunology, Stanford University School of Medicine,
Stanford, California 94305-5402; We have characterized the calcium response of a peptide-major histocompatibility complex
(MHC)-specific CD4+ T lymphocyte line at the single cell level using a variety of ligands,
alone and in combination. We are able to distinguish four general patterns of intracellular calcium elevation, with only the most robust correlating with T cell proliferation. Whereas all
three antagonist peptides tested reduce the calcium response to an agonist ligand, two give very
different calcium release patterns and the third gives none at all, arguing that (a) antagonism does not require calcium release and (b) it involves interactions that are more T cell receptor
proximal. We have also measured the time between the first T cell-antigen-presenting cell
contact and the onset of the calcium signal. The duration of this delay correlates with the
strength of the stimulus, with stronger stimuli giving a more rapid response. The dose dependence of this delay suggests that the rate-limiting step in triggering the calcium response is not
the clustering of peptide-MHC complexes on the cell surface but more likely involves the accumulation of some intracellular molecule or complex with a half-life of a few minutes.
Department of Chemistry, Stanford University School of
Medicine, Stanford, California 94305-5080; and the § Howard Hughes Medical Institute, Beckman
Center, Stanford University, Stanford, California 94305-5428
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