Figure 2.

Effector functions of inflammatory monocytes. In the absence of inflammation, bone marrow CCR2⁺ monocytes have an immature phenotype and are characterized by low levels of expression of MHC class II and costimulatory molecules. Following infection, monocytes are released into the peripheral circulation and migrate to sites of inflammation, where they express distinct effector phenotypes and undergo differentiation into DCs. The effector functions of CCR2⁺ monocytes are dictated by the inflammatory context and by the nature of the invading pathogen. (a) Following infection with L. monocytogenes, monocytes are first present in the marginal zone area of the spleen and subsequently migrate to the white pulp area, where bacterial lesions are established. Monocytes undergo differentiation into TipDCs and surround infected cells, thus preventing bacterial dissemination from the lesion. While most CCR2⁺ monocytes are not infected in vivo, monocytes in the peripheral circulation may become infected and transport bacteria to the CNS. (b) In the gastrointestinal tract, infection with S. typhimurium induces influx of inflammatory monocytes and their differentiation into TipDCs. (c) Although less is known regarding the function of monocytes during M. tuberculosis infection, they are recruited to the lung and may function as a source of nitric oxide (NO). (d ) During infection with T. gondii, inflammatory monocytes become directly infected and secrete IL-12 and NO and kill parasites. T. gondii–infected monocytes may also be involved in transport of parasites to the brain.