Abstract—Cytokines are critical for protection and pathogenesis in tuberculosis. In general, the T-helper (Th)1 and pro-inflammatory cytokines are considered to have a role in protection, and the anti- inflammatory and Th2 cytokines in susceptibility/pathogenesis of tuberculosis. To understand better the role of cytokines in tuberculosis, we have studied in vitro secretion of the above cytokines from the Peripheral Blood Mononuclear Cells (PBMCs) of tuberculosis patients (diabetic and non-diabetic) and healthy subjects. PBMCs were incubated in vitro with complex mycobacterial antigens and pools of peptides corresponding to M. tuberculosis -specific genomic Regions of Differences (RDs). The culture supernatants were assayed for the amount of cytokines released after 6 days of incubation. In general, the concentrations of antigen-induced Th2 cytokines were low/undetected and the pro-inflammatory cytokines were non-discriminatory. With respect to Th1 and anti-inflammatory cytokines, the antigens could be divided into three groups; the first with Th1-bias (culture filtrate of M. tuberculosis , RD1, RD5, RD7 and RD9), the second with anti-inflammatory-bias (whole bacilli and cell walls of M. tuberculosis , RD12 and RD13), and the third without any bias ( M. bovis BCG, RD4, RD10, RD6, RD11 and RD15). However, among the peptide pools, RD1 peptides induced strongest Th1-bias, and the addition of RD12 and RD13 peptides to PBMCs cultures inhibited the RD1-induced Th1-cell reactivity. The analyses of data for cytokines in diabetic and non-diabetic TB patients and healthy subjects showed a lower Th1:Th2/anti-inflammatory cytokines in diabetic TB patients, which may explain, at least in part, a faster deterioration in their clinical conditions.