In mice with tuberculosis, the disease lowered a key immune signal (IL‑2) and raised another (IL‑6). Giving standard antibiotics changed some of these signals, and adding an immune‑boosting treatment (likely thymalin) helped bring IL‑2 back up and further increased IL‑6 in certain immune cells. This shows the treatment can partly restore immune balance after infection, but the work was done in mice and not directly tested in people.

The authors investigated spontaneous and induced secretion of cytokins at different stages of generalized tuberculosis. In the development of infection there were inhibited IL-2 synthesis in response to ConA, emerging activity of PNO-alpha in response to the inductors in blood serum and culture of peritoneal macrophages, enhanced secretion of IL-6. Complete immunodeficiency was associated with cessation of IL-2 synthesis by splenocytes, elevated production of IL-6 by peritoneal macrophages, low concentrations of PNO-alpha in the serum and peritoneal macrophage cultures. In the treatment of M. bovis-infected mice with antibacterial drugs alone IL-6 secretion by peritoneal macrophages and PNO-alpha activity in the serum were increased. Immunocorrection resulted in marked activation of IL-2 production by splenocytes in response to ConA as well as enhanced synthesis of IL-6 in unstimulated cultures of peritoneal macrophages.