Mechanism of suppression of the depressed lymphocyte response in lung cancer patients.

We studied the function of monocyte-mediated suppression in the proliferative responses of depressed T-cells of patients with advanced lung cancer, with both local (Stage III) and extrapulmonary metastasis (Stage IV). The mononuclear cells of 13 non-treated patients showed a significant drop in proliferation upon stimulation with suboptimum, optimum and supraoptimum doses with regards to normal controls (p less than 0.001). On treating T-cells with indomethacin, lymphoblastic transformation increased in both groups (patients and controls), but was significantly greater in the patient group (p less than 0.001). The lipopolysaccharide (LPS) exerted an inhibitory effect on the suppressor cells of normal individuals, yet failed to do so in the case of patients treated either with or without indomethacin. The stimulation of the patients mononuclear cells with PWM failed to increase proliferation, and was not affected by either indomethacin of LPS. Our conclusions are as follows: Patients with lung cancer present a drop in mononuclear cell proliferation when stimulated with PHA; This phenomenon may be due to an exacerbation of the immune systems suppressor function; One of the suppressor mechanisms is prostaglandin-dependent and mediated by monocytes; The B-cells have no relevant functions.