series cells. These latter markers have recently been reviewed by Crocker and Burnett.2 The preparations usually bind to "X-hapten"-that is, 3-fucosyl-N-aretyllactosamine (3fNa) and include Leu Ml, 3C4, VEP8 and 9, and AGF 4.48.2 The epitopes labelled by these antibodies, however, are widespread in many tissues, including those of epithelial type.2 It is dangerous to presume that shared epitopes imply a common ontogeny, but, it would be interesting to speculate on a common ancestry between granulocytes and Reed-Sternberg and Hodgkin's cells. Accordingly, we applied two antisera to cathepsin G3 and leucocyte elastase4 to a series of 35 cases of confirmed Hodgkin's disease. These comprised seven each of: lymphocyte predominent, nodular sclerosing type 1 and type 2, mixed cellularity, and lymphocyte depletion Rye subtypes. The antibodies have been shown to be highly specific for granulocyte series cells of maturation stages from promyelocytes onwards, including some myeloblasts.34 Activity of cathepsin G has not been observed in other tissue types, and leucocyte elastase has only otherwise been seen in ileal epithelium.3 The antisera were applied to paraffin sections using standard indirect peroxidase, streptavidin-biotin, and immunogold-silver (IGSS) labelling methods.5 Mature granulocytes were intensely and consistently stained, but only very occasional ReedSternberg and Hodgkin's cells reacted; when this occurred, the staining was very weak, even with the IGSS method. In view of the high specificity of the antisera for granulocyte series cells and the high sensitivity of the IGSS method the findings suggested that if indeed Reed-Sternberg and Hodgkin's cells are related to granulocytes, then they share features only in terms of minor epitopes such as 3fNa, which, themselves, are expressed only on cells from the promyelocytic stage of differentiation.
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