e m c i

niv llon Review TRENDS in Parasitology Vol.23 No.7viral load is associated with a higher prevalence of leish-maniasis, and a lower CD4+ T-cell count is linked to visceral and disseminated forms of leishmaniasis [1,2]. It is also noteworthy that, in people infected with HIV-1, symptomatic leishmaniasis might represent reactivation of latent infection rather than primary infection [3]. So far, the presence of Leishmania and its antigens has been detected in macrophages (MØ), dendritic cells (DCs) (Box 1), polymorphonuclear leukocytes, eosinophil gra-nulocytes and fibroblasts [4]. However, HIV-1 has also been shown to interact with several cell types, such as CD4+ T lymphocytes, glial cells, bone marrow cells, DCs, monocytes andMØ [5]. Interestingly, a latent infection can be established following a primary infection with each human pathogen. Based on the idea that they can infect the same cell types, namely MØ and DCs, it is proposed HIV-1 can be found inside DCs. These two pathogens can modify the physiological functions of DCs for their own survival and propagation. For example, production of cyto-kines, expression of certain receptors and adhesion mol-ecules, as well as DC maturation and migration can be altered as a result of the presence of these microorganisms in DCs. The reported Leishmania- and HIV-1-mediated effects on cytokine production and cell-surface expression of different receptors in DCs will be described herein. The putative interactions between Leishmania and HIV-1 that might occur in DCs will also be discussed. It is important to emphasize that the published Leishmania-related literature is founded on studies that have used different experimental methodologies (e.g. mouse versus human experimental model systems, differ-ent sites of injection, different DC subsets, immature versus mature DCs and various Leishmania species). The same applies to HIV-1 studies, where distinct viral strains have been used and methods to derive/isolate DCs might result in the production of different DC subset