Host Defense Mechanisms in Secondary Syphilitic Lesions

Cell-mediated immunity is thought to be of critical importance in antisyphilitic host defense, but the exact mechanisms are still unknown. This fact is particularly true for HIV-infected persons with a deficit in CD4+ T-cell number. We therefore obtained lesional skin samples from HIV+ and HIV− patients with secondary syphilis at different time points of lesional age to search both for causative microorganisms and to characterize the inflammatory infiltrate. By doing so, we detected Treponema pallidum spirochetes with a much greater abundance in late lesions of HIV+ individuals compared with the HIV− cohort. The dominating inflammatory cells were T cells, macrophages, and neutrophils at all stages and plasma cells in older lesions. In HIV− persons, T cells consisted of equal numbers of CD4+ and CD8+ T-cells, whereas in HIV+ patients, the majority of T cells belonged to the CD8 lineage and produced both IFN-γ and IL-17. Regulatory T cells and Langerhans cells were reduced in these patients compared with their HIV− counterparts. Because of our observations, we propose that T cells of both the CD4 and CD8 lineage are needed for an at least partial protective antisyphilitic immunity. Compensation mechanisms in HIV+ individuals, such as an increase of Tc1/17 cells as well as a reduction in immunoregulatory Langerhans cells and T cells, apparently do not overcome the deficiencies in these patients to eliminate the spirochete.