Chlamydia pneumoniae infection has long been suspected as a possible cause of atherosclerosis and has been frequently detected in atheromatous plaques of the coronary arteries. Nevertheless, its distribution is not correlated to the severity or extent of the disease, but it would support the hypothesis that the organism may be an active factor in the pathogenesis of atherosclerosis. A group of patients with stable angina were examined as to whether or not the positivity of antibodies against Chlamydia pneumoniae modified cellular populations as mechanisms responsible for the alterations of inflammatory response. We concluded that the presence of IgG anti-C. pneumoniae antibodies do not participate in the activation of inflammatory mechanisms that may intervene in the genesis of atherosclerosis in patients with stable angina.