Twenty years ago, R. Steinman and colleagues established that dendritic cells (DCs) have unique capacities to prime naive T cells and that DC maturation is the checkpoint for the initiation of adaptive immune responses (1–3). In the mid-1990s, C. Janeway pointed out the pivotal role of innate effectors in dictating adaptive immune responses while few researchers wondered why antigens were much more immunogenic for the specific immune system when applied with “adjuvants” that stimulated innate immunity (4). DC “maturation” appears to be the cornerstone between innate and cognate immunity, but what regulates DC maturation? DCs are sensors of infection and danger (5) and pathways leading to DC activation involve at least toll like receptors and/or proinflammatory cytokine and chemokine receptors (4, 5). However, in non-microbial scenarios such as tumorigenesis, transplantation, or atopy, DC activation...

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