BACKGROUNDS: Atherosclerosis is an inflammatory disease and it is developed by the dysregulation of T-cell derived cytokine. Recently, CD4(+) T-helper cell producing Interleukin-17 (Th17) and interferon-gamma (Th1) has been investigated in some vascular disease, however, their role and level of expression are not certain in specific coronary artery disease. Thus, we analyzed the Th17 and Th1 cell responses in patients with stable angina (SA), acute coronary syndrome (ACS) with the technique of flow cytometry manner. METHODS: We included 133 patients with chest pain and peripheral artery blood was sampled during conventional coronary angiography. Mononuclear cells from patients were stimulated for 4 hours ex vivo with phorbol myristate acetate and ionomycin. The frequencies of Th17 and Th1 were measured by flow cytometry. Expressions of T cell associated chemokine receptors (CCR4, CCR6, CXCR3) were assessed after the stain with specific antibodies by same manner. RESULTS: Patients were divided into a control (non cardiac chest pain) group (26 patients), SA group (44 patients) and ACS group (63 patients). There was no significant difference in baseline characteristics including age, sex, and cardiovascular risk factors between groups. WBC count in ACS group (9030.0짹3753.8/mm쨀) significantly increased comparing control and SA group (6680.4짹2101.6/mm쨀, 6551.8짹1480.0/mm쨀, respectively, p<0.05), however, the frequencies of lymphocyte were not different between groups (control: 33.5짹10.4%, SA: 32.8짹8.7%, ACS: 32.3짹12.9%). Patients in SA group showed higher frequency of Th17 cell (3.1짹1.2%) compared with patients with control (1.9짹1.0%) and ACS (1.8짹1.1%) group, and it was statistically significant (p<0.05). The frequency of Th1 cell was also highest in SA groups (control: 16.0짹8.4%, SA: 22.7짹9.7%, ACS: 15.3짹11.1%, p<0.05). The frequency of CXCR3(+) was highly correlated with Th1 and it was highest in SA group (control: 22.7짹10.2%, SA: 31.0짹11.6%, ACS: 22.2짹11.6%, p<0.05). CCR4(+)CCR6(+) was closely related with Th17 cell and it significantly increased in SA group (control: 10.6짹2.9%, SA: 13.6짹5.0%, ACS: 12.0짹3.7%, p<0.05). CONCLUSIONS: The T-cell derived inflammatory mechanism can be different between ACS and SA groups. Increased Th17 and Th1 cell response was more important in the pathogenesis of SA than in ACS.