Abstract
We demonstrated that CD4+ αβ (CD4+) and γδ T cell subsets from healthy donors had similar effector functions (cytotoxicity and cytokine production) in response to mycobacterial antigens, despite differences in the antigens recognized. To elucidate the pathogenesis of pulmonary tuberculosis, this study was undertaken to compare T cell functions between patients with pulmonary tuberculosis with no complications and healthy controls.
Both resting and activated CD4+ and γδ T cells from the patient group proliferated in response to live BCG at a significantly lower rate than those from the control group. The cytotoxicity of BCG-pulsed monocytes and IFN-γ production in both the CD4+ and γδ T cells from patients was significantly lower than those of controls. In contrast to IFN-γ, significantly higher IL-10 production by both CD4+ and γδ T cells from patients was detected. The proliferative responses to BCG by CD4+ and γδ T cells from patients after antituberculous therapy were partially restored, but remained at lower levels compared with controls.
These results suggest that not only a general deterioration in CD4+ and γδ T cells effector functions, but also suppressive factors (such as IL-10) might be responsible for the pathogenesis of pulmonary tuberculosis, and that the low response to BCG by both CD4+ and γδ T cells in patients with tuberculosis is in part attributable to patient predisposition.
