Adenosine deaminase isozymes in tuberculous pleural effusion

Total adenosine deaminase (ADA) activity and its isozyme (ADA1 and ADA2) activities were measured in pleural effusions and serum samples from patients with tuberculosis and in those from patients with lung cancer as controls. To analyze the cellular source of ADA isozymes in tuberculous pleural effusions, ADA isozyme activities in CD2+ T lymphocytes purified from tuberculous pleural effusions and cultured human cell lines derived from hematopoietic tumors were measured. Tuberculous pleural effusions had a much higher ADA activity than cancerous effusions, and high ADA activity mainly originated from the increase in ADA2 activity. Further, total ADA activity in tuberculous pleural effusions decreased after antituberculosis treatment, because of the decrease in ADA2 activity. On the other hand, measurement of ADA and ADA isozyme activities in T lymphocytes purified from tuberculous pleural effusions and human hematopoietic cell lines showed dominant expression of ADA1 in total ADA activity. In conclusion, we found that ADA2 is a dominant component of tuberculous pleural effusions and that ADA1 is a major component of lymphoid cells. These results suggest that elevation of ADA activity in tuberculous pleural effusions does not always reflect the activation of cell-mediated immunity.