Lymphokines (LCL-LK) prepared from the human lymphoid cell line RPMI 1788 were injected intradermally into tumour-bearing patients. Biopsies of skin reactions were obtained for histological study from 30 min. to 72 hr, and for comparison, biopsies were taken at similar times of tuberculin reactions in tuberculin-positive patients. The early response to LCL-LK consisted of polymorph adherence to vascular endothelium (at 30 min.) followed by polymorph exudation, oedema and haemorrhage (1-2 hr); mononuclear and eosinophilic leucocyte emigration began at 4 hr; and by 12 hr, when the reaction was maximal clinically, there was widespread pleomorphic leucocytic infiltration of the dermis. At later times (48-72 hr) skin reactions to LCL-LK showed predominantly mononuclear cell infiltration and hypertrophy of vascular endothelium. Electron microscopy at 48 hr revealed perivascular lymphocytes and macrophages. The skin reaction to LCL-LK appeared to superimpose an early component of marked polymorph infiltration, oedema and haemorrhage upon a mononuclear cell exudation similar to that seen in the tuberculin reaction. It was concluded that the later phase of the skin reaction to lymphoid cell line lymphokine in the human bore a close histological similarity to the established tuberculin reaction. The LCL-LK reaction occurred in patients anergic to recall antigens. Its intensity was mainly related to dose and did not vary substantially between different batches of lymphokines.

Lymphokines (LCL-LK) prepared from the human lymphoid cell line RPMI 1788 were injected into dermal nodular metastases of three patients with advanced breast carcinoma anergic to recall antigen (tuberculin). Three different injection schedules were employed. Ten such nodules were examined by excision biopsy and their histological appearances were compared with biopsies of four further nodules not injected with the lymphokine. Intranodular injection of LCL-LK resulted in clinical regression of tumour and histological evidence of tumour-cell necrosis with pleomorphic leucocytic infiltration by polymorphs, macrophages and lymphocytes. Electron microscopy of two such nodules failed to show close cell contact between leucocytes and tumour cells prior to tumour-cell necrosis. This study extends evidence that injection of inflammatory lymphokines into accessible tumour can result in local tumour regression and it suggests that such tumour-cell destruction may be the result of a variety of factors operating during local inflammatory response.

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