The relationship of the production of interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha) and interleukin-2 (IL-2) to the pattern and etiology was studied in patients with pulmonary tuberculosis (n = 74) and nontuberculous lung diseases (n = 28). There was an inverse correlation between the production of the proinflammatory cytokines IL-1 beta and TNF-alpha and the main T-cellular immunity IL-2. An exacerbation of a tuberculous process is accompanied by an increase in IL-1 beta and TNF-alpha productions and by a decrease in inducted IL-2 synthesis. With favourable changes, there was, on the contrary, a reduction in the levels of IL-1 beta and TNF-alpha and a rise in IL-2. There were differences in the rate of cytokine synthesis in pulmonary tuberculosis, lung cancer, and pneumonia. Patients with cancer are most typified by the spontaneous mononuclear production of serum TNF-alpha and by the low level of IL-2 when PGA is stimulated. On the contrary, the least TNF-alpha synthesis and pronounced IL-2 production in pneumonia. A combination of the high production of PPD-induced IL-1 beta and PGA-stimulated IL-2 is more specific to patients with infiltrative pulmonary tuberculosis.

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