Mononuclear cell subsets in the nickel-allergic reaction in vitro and in vivo.

Nickel is the major cause of metal-induced contact allergy. To understand the mechanism of its immune reaction, we studied changes in lymphocyte surface markers during nickel challenge in both allergic and healthy subjects using an in vitro nickel reaction in which the lymphocytes of allergic subjects divide when they are stimulated with nickel sulfate. The lymphocytes were labeled with monoclonal antibodies (MAbs) to cell-surface antigens and studied by flow cytometry. Mononuclear cells from the nickel reaction in vivo were studied from skin biopsy specimens using MAbs and avidin-biotin immunohistochemistry. Nickel-induced lymphoblast transformation occurred in vitro only in cells from nickel-allergic subjects. CD4+ cells and CD45RO+ cells were overrepresented among the lymphoblasts of nickel-sensitive subjects, whereas CD8+ and CD8+CD11b+ and CD4+CD45R+ cells were underrepresented. The lymphoblasts contained T cells with the following activation markers: CD25, HLA-DR, CD26, CD71, Ki-67, and activation-associated antigen detected by the MAb, M21C5, but they were CD30-. CD16+ cells were overrepresented among the lymphoblasts. Nickel-reacting T cells used predominantly the T cell receptor, alpha beta-heterodimer, but no preferential selection of either V beta 5, V beta 6, or V beta 8 was observed. The phenotypes of nickel-reacting cells from cutaneous biopsy specimens were in agreement with the in vitro results.