Human atherosclerotic lesions contain macrophages and CD4⁺ T cells [1]. The antibody response to modified lipids found in atherosclerosis seems to be characteristic of the disease. The challenge is to elucidate how the immune system influences atherogenesis in relation to classic risk factors for atherosclerosis [2].

We compared lymphocyte subsets of patients with severe atherosclerosis (17 with coronary artery disease and 11 with peripheral vascular disease) before bypass surgery with subsets in a control group (15 patients without atherosclerosis or with nonsignificant atherosclerosis in whom valvular disease was investigated by coronary angiography and vascular ultrasonography). The two groups were paired by age and sex (mean age ±SD, 62 ± 14 years; 90% men).

One day before the intervention, we considered the distribution of lymphocytes that bore the following antigens: CD3⁺; CD3⁺ and CD4⁺; CD3⁺ and CD8⁺; and CD3⁺, CD16⁺, and CD56⁺. No patient was seropositive for human immunodeficiency virus or hepatitis B or C virus; none had infection; and none had had myocardial infarction or surgical intervention within 3 months of study entry. Patients with severe cardiac and hepatic insufficiency, autoimmune disease, and rheumatoid disease were excluded. Data were acquired on the FACSAN immunocytometry system (Becton Dickinson, Mountain View, California). Reagents used were monoclonal antibodies (Opticlone kit, Immunotech, Marseille, France). We compared the two groups by using analysis of variance (Fischer exact test).

Results are shown in Table 1. The absolute natural killer cell count was higher (P < 0.05) in patients with severe atherosclerosis (that is, coronary artery disease and peripheral vascular disease) before bypass surgery than in the control group before valvular replacement. The absolute B-cell count was higher only in patients with peripheral vascular disease (P < 0.05). The difference between other lymphocytes subsets was not significant.

Psychological stress induces neuroimmunomodulation, particularly by modification of natural killer cells [3]. We assume that the stress before the intervention was the same in both groups but that the immune reactivity was different in patients with vascular disease. Natural killer cells [4] may be involved in severe atherosclerosis as macrophages and CD4⁺ T cells.