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D. I. Beller is the first author of a 1982 study relating Mac-1 to a specific function of the complement system. The investigators used an antibody against Mac-1 and a rosette assay, in which appropriately coated red blood cells bind around immune cells. The antibody inhibited binding mediated by the complement fragment iC3b, while selected other receptor-dependent binding remained intact.^[ref]

The controls separated selective inhibition from indiscriminate loss of cell binding. The original conclusion was that Mac-1 was identical to, or closely associated with, the relevant complement-receptor function. A blocking experiment can establish a strong functional association without, by itself, resolving every molecular detail of that association.^[ref]

T. A. Springer contributed to experiments connecting immune-cell surface proteins with recognition and cell adhesion. In a 1982 study with D. I. Beller and collaborators, selective antibody blocking related Mac-1 to binding of targets bearing iC3b, a fragment involved in the complement system.^[ref]

With M. L. Dustin, T. A. Springer later investigated how stimulating the T-cell receptor changes adhesion through LFA-1. The 1989 experiments found a rapid, transient increase in adhesion strength. This supplied a mechanism for coordinating target recognition with sticking and subsequent release, rather than treating the presence of an adhesion protein as a fixed measure of how strongly a cell will bind.^[ref]