NICKEL ANTIGEN INDUCES IL-2 SECRETION AND IL-2 RECEPTOR EXPRESSION MAINLY ON CD4+ T-CELLS, BUT NO MEASURABLE GAMMA INTERFERON SECRETION IN PERIPHERAL-BLOOD MONONUCLEAR CELL-CULTURES IN DELAYED-TYPE HYPERSENSITIVITY TO NICKEL

Abstract

Nickel sulphate antigen-induced peripheral blood lymphocyte activation in vitro was characterized by lymphokine measurement (IL-2, IFN-.gamma.) and phenotyping of the IL-2 responsive cells. Mononuclear cells from nickel-sensitive patients synthesized more DNA, produced more IL-2 and had more IL-2 receptor positive cells in response to nickel than did those of the control subjects. On the other hand no IFN-.gamma. was detectable in the nickel supernatants, while PPD, used as the control antigen, induced pronounced quantities of IFN-.gamma. with an equal amount of DNA synthesis. The increase in IL-2 receptor positive cells was due to activation of CD4+ (helper/inducer) T cells. T cells with HLA-DR antigen surface markers were more numerous on each day of culture than cells with IL-2 receptors. These two activation markers were co-expressed on the same cells only to a certain extent, thus perhaps reflecting different types or phase of activation. In conclusion, nickel-induced peripheral blood mononuclear cell activation in vitro differs from microbial antigen-induced activation with respect to its modest or non-existent IFN-.gamma. response.