Background: Cardiovascular disease accounts for an estimated 40% of all deaths in New Zealand, with atherosclerosis as the underlying aetiology in the vast majority of cases. Deaths are higher among Maori compared with non-Maori, especially those under the age of 65 years. The importance of the role of infection and inflammation in atherosclerosis is widely accepted, and there has been increasing awareness that immune responses are central to atherogenesis. Chronic inflammatory periodontal disease is among the most common infections, with over 10% of New Zealanders at risk of losing teeth. A number of studies have shown associations between periodontal diseases and an increased risk of stroke and coronary heart disease. While it is recognised that large-scale intervention studies are required, studies showing the pathogenic mechanism are still needed to establish the biological rationale underlying the relationship between these two chronic diseases. Objective: The objective of the present study was to determine the profile of cytokine gene expression of P. gingivalis GroEL reactive T cells in the peripheral blood of patients with atherosclerosis and those with chronic periodontitis. In this way some insight may be gained into the functional activity of these cells in atherosclerosis and chronic periodontitis. Methods: Peripheral blood was obtained from five atherosclerosis, five chronic periodontitis, and two healthy patients plus one patient with atherosclerosis with chronic periodontitis. Mononuclear cells were isolated using density gradient centrifugation. The mononuclear cells were cultured in media alone and with recombinant P. gingivalis GroEL to determine the lymphoproliferative activity in each group. RNA extraction was performed and followed by real time PCR to determine the cytokine gene expression profiles of atherosclerosis and chronic periodontitis patients. The results were analysed using the 2-ΔΔCt method. Results: A variation of lymphoproliferative activity was observed in atherosclerosis and chronic periodontitis. Differential cytokine gene expression profiles were observed in the atherosclerosis and chronic periodontitis groups. Thirty-nine (46%) of 84 genes were differentially expressed in the atherosclerosis group, and fifty-five (65%) of 84 genes were differentially expressed in the chronic periodontitis group. Of the thirty-nine genes that were differentially expressed in the atherosclerosis group, nineteen (49%) were upregulated and twenty (51%) were downregulated. On the other hand, in the chronic periodontitis group, of the fifty-five genes that were differentially expressed, twenty-eight (51%) genes were upregulated, and twenty-seven (49%) genes were downregulated. Conclusion: The results suggest that GroEL-specific T cells may respond differently in atherosclerosis and chronic periodontitis. The reason for this difference is unknown but may relate to the recognition of different epitopes in each group. This remains to be determined. Keywords: Atherosclerosis, GroEL, Periodontitis