Aspirin-like drugs prime human T cells: Modulation of intracellular calcium concentrations

E. Flescher, D. Fossum, P. J. Gray, G. Fernandes, M. J.K. Harper, N. Talal

Research output: Contribution to journalArticlepeer-review

59 Scopus citations


Aspirin-like drugs (ALD) enhance T cell proliferation by suppressing PG production in monocytes. Normal human T cells do not produce any eicosanoids. Therefore we studied whether ALD would affect purified T cells directly. We found that ALD enhanced the proliferation and IL-2 production of T cells in the absence of monocytes. This effect did not depend on arachidonic acid metabolism as no lipoxygenase products and only nonsuppressive levels of cyclooxygenase products were detected in T cell cultures. Several possible mechanisms of the ALD effect were ruled out including 1) enhanced mitogen binding, 2) induction of activation markers (IL-2R, transferrin receptor, HLA-DR) on the cell surface, 3) down-regulation of suppressor cells. ALD caused a rise in [Ca2+](i) which appeared to reflect an influx of Ca2+ from the extracellular milieu and was more pronounced in CD4+ cells. The rise in intracellular levels of Ca2+, that is considered a necessary second messenger for T cell activation, may prime these cells for an enhanced response to mitogens. In addition, ALD increased T cell membrane fluidity but only at higher concentrations than those found to enhance proliferation. The pharmacologic effect of ALD on T cells presents a possible new immunoenhancing potential of these drugs and may have therapeutic use in immunosuppressed individuals.

Original languageEnglish (US)
Pages (from-to)2553-2559
Number of pages7
JournalJournal of Immunology
Issue number8
StatePublished - 1991

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


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