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Prostaglandin E₂ Selectively Inhibits Human CD4⁺ T Cells Secreting Low Amounts of Both IL-2 and IL-4¹

Xiaowen He^2, and John M. Stuart^*,

^* Research Service 151, Veterans Administration Medical Center, and Department of Medicine, University of Tennessee, Memphis, TN 38104

PGE₂ is a potent inflammatory mediator with profound immune regulatory actions. The present study examined the effects of PGE₂ on the activation/proliferation of CD4⁺ T cells using 37 cloned CD4⁺ T cell lines. Ten T cell clones sensitive to PGE₂ and 10 T cell clones resistant to PGE_2, as measured by proliferation in response to anti-CD3 Ab, were selected for comparison. It was found that the PGE₂-sensitive T cells were characterized by low production (<200 pg/ml) of both IL-2 and IL-4, while PGE₂-resistant T cells secreted high levels (>1000 pg/ml) of IL-2, IL-4, or both. The roles of IL-2 and IL-4 were confirmed by the finding that addition of exogenous lymphokines could restore PGE₂-inhibited proliferation, and PGE₂-resistant Th1-, Th2-, and Th0-like clones became PGE₂ sensitive when IL-2, IL-4, or both were removed using Abs specific for the respective lymphokines. In addition, we showed that the CD45RA expression in PGE₂-sensitive T cells was significantly lower than that in PGE₂-resistant cells (mean intensity, 1.2 ± 0.6 vs 7.8 ± 5.7; p = 0.001). In contrast, CD45RO expression in PGE₂-sensitive T cells was significantly higher that that in PGE₂-resistant cells (mean intensity, 55.7 ± 15.1 vs 33.4 ± 12.9; p = 0.02). In summary, PGE₂ predominantly suppressed CD45RA^-RO⁺ CD4⁺ T cells with low secretion of both IL-2 and IL-4.

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