One of the first steps in the development of atherogenesis is adhesion of circulating monocytes to the vascular endothelium that is stimulated by beta(2)-integrins. Stress has been associated with enhanced expression of beta(2)-integrins on monocyte cell surface (Greeson et al., 2008). Central nervous system (CNS) serotonin regulates aspects of the stress response that can influence inflammatory processes that increase risk for atherosclerosis. This study examines effects of an environmental stressor (indexed by socioeconomic status (SES)) and CNS serotonin (indexed by CSF 5HIAA level), on the expression of beta(2)-integrins (CD11a, CD11b, and CD11c) on circulating monocytes in 131 volunteers. Participants completed a protocol consisting of a lumbar puncture for assessment of CSF 5HIAA levels (day 1) followed by an experimental protocol (day 2). Blood samples for the present analyses were obtained at baseline on day 2. The interaction of SES x 5HIAA was a significant predictor of levels of CD11b and CD11c expression (p=.02, and p=.05, respectively); the mean CD11b difference between Hi and Lo SES subjects was significant (p=.003) only in those with Lo levels of 5HIAA, while SES differences in CD11b among those with Mid and Hi levels of 5HIAA did not vary statistically. The pattern of findings was similar for CD11c. The present results suggest that the combination of high environmental stress and low CNS serotonin function could contribute to atherogenesis through processes that lead to increased expression of the beta(2)-integrins CD11b and CD11c on monocyte cell surfaces.