Migration of antigen (Ag)-loaded dendritic cells (DCs) from sites of infection into draining lymphoid tissues is fundamental to the priming of T-cell immune responses. We evaluated monocyte-derived DCs (MoDCs) and peripheral blood DCs (PBDCs) to respond to proinflammatory mediators, CD40L, and intact bacteria. All classes of stimuli induced DC phenotypic maturation. However, for MoDCs, only prostaglandin E₂ (PGE₂)–containing stimuli induced migratory-type DCs. Thus, immature MoDCs that encountered proinflammatory cytokines or CD40L or intact bacteria in the presence of PGE₂ acquired migratory capacity but secreted low levels of cytokines. Conversely, MoDCs that encountered pathogens or CD40L alone become nonmigratory cytokine-secreting cells (proinflammatory type). Interestingly, both migratory- and proinflammatory-type DCs expressed equivalent levels of chemokine receptors, suggesting that the role of PGE₂ was to switch on migratory function. We demonstrate that PGE₂ induces migration via the E-prostanoid 2/E-prostanoid 4 (EP₂/EP₄) receptors and the cAMP pathway. Finally, migratory-type MoDCs stimulated T-cell proliferation and predominantly IL-2 secretion, whereas proinflammatory-type MoDCs induced IFN-γ production. In contrast, CD1b/c⁺ PBDC rapidly acquired migratory capacity irrespective of the class of stimulus encountered and secreted low levels of cytokines. This suggests that not all mature stages of DCs are destined to migrate to lymphoid organs and that the sequence in which stimuli are encountered significantly affects which functions are expressed. Thus, certain immature DC subsets recruited from the resting precursor pool may have multiple functional fates that play distinct roles during the induction and effector phases of the immune response. These findings have important implications for the clinical utility of DCs in immunotherapy.

Individuals with cancer and their families assume responsibility for management of cancer as an acute and chronic disease. Yet, cancer lags other chronic diseases in its provision of proactive self-management support in routine, everyday care leaving this population vulnerable to worse health status, long-term disability, and poorer survival. Enabling cancer patients to manage the medical and emotional consequences and lifestyle and work changes due to cancer and treatment is essential to optimizing health and recovery across the continuum of cancer. In this paper, the Global Partners on Self-Management in Cancer puts forth six priority areas for action: Action 1: Prepare patients and survivors for active involvement in care; Action 2: Shift the care culture to support patients as partners in cocreating health and embed self-management support in everyday health-care provider practices and in care pathways; Action 3: Prepare the workforce in the knowledge and skills necessary to enable patients in effective self-management and reach consensus on core curricula; Action 4: Establish and reach consensus on a patient-reported outcome system for measuring the effects of self-management support and performance accountability; Action 5: Advance the evidence and stimulate research on self-management and self-management support in cancer populations; Action 6: Expand reach and access to self-management support programs across care sectors and tailored to diversity of need and stimulation of research to advance knowledge. It is time for a revolution to better integrate self-management support as part of high-quality, person-centered support and precision medicine in cancer care to optimize health outcomes, accelerate recovery, and possibly improve survival.