Regulation of interleukin 3 gene induction in normal human T cells.

S C Guba; G Stella; L A Turka; C H June; C B Thompson; S G Emerson

doi:10.1172/JCI114352

Howard Hughes Medical Institute, University of Michigan, Ann Arbor 48109.

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Howard Hughes Medical Institute, University of Michigan, Ann Arbor 48109.

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Howard Hughes Medical Institute, University of Michigan, Ann Arbor 48109.

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Howard Hughes Medical Institute, University of Michigan, Ann Arbor 48109.

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Published in Volume 84, Issue 6 on December 1, 1989
J Clin Invest. 1989;84(6):1701–1706. https://doi.org/10.1172/JCI114352.
© 1989 The American Society for Clinical Investigation

Published December 1, 1989 - Version history

The regulation of IL-3 gene induction in human peripheral blood T cells was studied. IL-3 gene expression was inducible by crosslinking of the T cell receptor/CD3 complex using anti-CD3 MAb G19-4. Anti-CD3-induced IL-3 gene expression was found to be limited to the CD28+ T cell subset and could be augmented by costimulating T lymphocytes with antibodies directed against CD28. IL-3 expression could also be induced by costimulation of T cells with both phorbol ester and ionomycin, which are thought to mimic the intracellular effects of T cell receptor-antigen interaction. However, unlike other lymphokines such as IL-2 or granulocyte-macrophage colony-stimulating factor, IL-3 gene expression is not induced by stimulation of cells with phorbol myristate acetate and anti-CD28. We conclude that IL-3 gene regulation is under stringent control since IL-3 gene expression occurs only in the CD28+ subset of T cells, and since IL-3 induction obligately requires increased intracellular calcium.

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