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In the ‘1980s, the pathologic role of IL-1 and TNF alpha became evident and, among several ideas, one was to reduce or eliminate cytotoxic T cell-dependent autoimmune diseases by using either monoclonal antibodies to T cell surface molecules, such as CD3, CD4, and CD52 or IL 2-diphtheria-toxin fusion protein that, after uptake, would kill the cell
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