Lymphotoxin formation by lymphocytes and muscle in polymyositis.

Muscle pieces from 11 patients with dermatomyositis or polymyositis were incubated with autologous peripheral blood lymphocytes and the supernates examined for the production of lymphotoxin, a mediator of delayed hypersensitivity, using human fetal muscle monolayers as the target cell. In the case of all 10 active patients, production of lymphotoxin was demonstrated. This mediator was also demonstrated when muscle alone was incubated from two patients with extensive cellular infiltration. Lymphotoxic activity was not found in supernates obtained by incubation of muscle from nine control subjects with their autologous peripheral blood lymphocytes. Addition of methyl prednisolone to active cultures inhibited the action of lymphotoxin on the muscle monolayers. Lymphotoxin was not demonstrated when breast tumor tissue from a patient with dermatomyositis was incubated with autologous lymphocytes. The lymphotoxic agent in the active supernates had similar chromatographic properties to those of a sample of purified lymphotoxin. These findings suggest that muscle injury in polymyositis is a result of a cellular immune response to an antigen present in involved muscle tissue.