Interleukin-2 (IL-2) induces T cell proliferation in an autocrine manner and provides a means by which antigen triggered T cells can be clonally expanded in vitro. During the following activation, the activity of IL-2 is mediated by specific high affi...
Interleukin-2 (IL-2) induces T cell proliferation in an autocrine manner and provides a means by which antigen triggered T cells can be clonally expanded in vitro. During the following activation, the activity of IL-2 is mediated by specific high affinity IL-2 binding membrane receptors which are expressed shortly after activation. In this process, a 42 KD-fragment (soluble IL-2R) is continuously cleaved off and circulates as a soluble marker of T lymphocyte activation. Elevated level of soluble IL-2R has been identified in the serum of patients with malignant autoimmune and allergic disorders, systemic parasitic infection, undergoing graft versus host disease, acute or chronic lymphocytic leukemia and HIV-infection. ADA (adenosine deaminase) completes the process of differentiation of T cell and is essential for progression of T cell maturation. Therefore level of ADA is to correlated with magnitude of T cell immune response. The fact that expression of sIL-2R and ADA activity increases in peripheral blood T-lymphocytes of patients with active pulmonary tuberculosis suggests that T cell activation might have a major role in the pathogenesis of pulmonary tuberculosis. In order to evaluate the T cell immune response in pulmonary tuberculosis, we measured the serum concentration of sIL-2R and ADA activity in 17 patients with current pulmonary tuberculosis, 10 chronic inactive pulmonary tuberculosis, 10 as normal controls.
(1) Current pulmonary tuberculosis had significantly higher levels of sIL-2R (237.24±95.47)when compared with those of inactive tuberculosis (78.6±11.06). and the control (68.17±15.4) group.
(2) ADA activity in current pulmonary tuberculosis was significantly increased (34.41±20.63) when compared with those of inactive tuberculosis (24.7±14.36) and control (17.65± 5.94) group.
(3) There was good correlation between sIL-2R concentration and ADA activity in serum in current pulmonary tuberculosis group.
(4) sIL-2R concentration and ADA activity was decreased significantly 6 months after anti-tuberculosis drug medication.
In conclusion, sIL-2R concentration and ADA activity in serum in current pulmonary tuberculosis group was increased when compared with those of inactive pulmonary tuberculosis and the control group.
By the way, T cell mediated immune response was enhanced in current pulmonary tuberculosis, but in inactive chronic pulmonary tuberculosis who had treated by antituberculosis drug medication, the concentration of sIL-2R and ADA activity was nearly normal.