The effect of rTNF-α on human T cell function was examined and compared with that of rIL-1β by assessing the ability of each cytokine to support mitogen-induced proliferation, IL-2 production, and IL-2R expression. TNF-α and IL-1β each enhanced DNA synthesis induced by PHA or immobilized mAb to the CD3 molecular complex. In addition, each cytokine increased the number of cells entering the G1 phase of the cell cycle and augmented IL-2R expression. The combination of optimal concentrations of these factors supported these responses to a greater extent than either cytokine alone, suggesting that T cell responsiveness is independently regulated by the action of at least two separate monocyte derived cytokines. Whereas TNF-α had little effect, IL-1β augmented IL-2 mRNA expression and IL-2 production by mitogen-stimulated cells. Furthermore, IL-1β enhanced proliferation with increasing length of culture. Whereas TNF-α also enhanced proliferation late in culture, it was less effective in this regard than IL-1β. Thus, IL-1β and TNF-α augment mitogen-induced T cell proliferation by increasing the number of cells initially activated and by promoting subsequent cell cycle progression. They differ, however, in their capacity to promote IL-2 mRNA and IL-2 production and therefore ongoing T cell proliferation.
|Original language||English (US)|
|Number of pages||6|
|Journal||Journal of Immunology|
|Publication status||Published - 1988|
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