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* Cancer Immunotherapy and Gene Therapy Program, Clinical Immunology Unit, H. San Raffaele Scientific Institute, Milan, Italy; Molmed SpA, Milan, Italy; Department of Internal Medicine III, Institute for Clinical Immunology and Rheumatology, Friedrich Alexander University, Erlangen-Nuremberg, Germany; Departments of Medicine I and Neurology, University of Heidelberg, Heidelberg, Germany; ¶ German Cancer Research Center, Heidelberg, Germany; and || Chromatin Dynamics Unit and # Vita-Salute San Raffaele University, Milan, Italy
High mobility group box 1 (HMGB1) is an abundant and conserved nuclear protein that is released by necrotic cells and acts in the extracellular environment as a primary proinflammatory signal. In this study we show that human dendritic cells, which are specialized in Ag presentation to T cells, actively release their own HMGB1 into the extracellular milieu upon activation. This secreted HMGB1 is necessary for the up-regulation of CD80, CD83, and CD86 surface markers of human dendritic cells and for IL-12 production. The HMGB1 secreted by dendritic cells is also required for the clonal expansion, survival, and functional polarization of naive T cells. Using neutralizing Abs and receptor for advanced glycation end product-deficient (RAGE–/–) cells, we demonstrate that RAGE is required for the effect of HMGB1 on dendritic cells. HMGB1/RAGE interaction results in downstream activation of MAPKs and NF-
B. The use of an ancient signal of necrosis, HMGB1, by dendritic cells to sustain their own maturation and for activation of T lymphocytes represents a profitable evolutionary mechanism.
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