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The adapter protein ADAP is required for selected dendritic cell functionsKeywords: Adapter protein, ADAP, Dendritic cell, Integrin, Inside-out signaling Abstract: ADAP-deficient BMDCs showed almost normal levels of antigen uptake, adhesion, maturation, migration from the periphery to the draining lymph nodes, antigen-specific T-cell activation, and production of the proinflammatory cytokines IL-6 and TNF-∝. Furthermore, we provide evidence that the activation of signaling pathways after lipopolysaccharide (LPS) stimulation are not affected by the loss of ADAP. In contrast, ADAP-deficient BMDCs showed defects in CD11c-mediated cellular responses, with significantly diminished production of IL-6, TNF-∝ and IL-10. Actin polymerization was enhanced after CD11c integrin stimulation.In summary, we propose that the adapter molecule ADAP is critical for selected CD11c integrin-mediated functions of dendritic cells.Adapter molecules mediate protein-protein interactions in signal transduction cascades. These signaling cascades translate information from cell surface receptors into cellular responses. We focused our research on the adapter molecule ADAP (adhesion and degranulation promoting adapter protein). To investigate the function of ADAP in immune cells we used a genetically engineered mouse lacking this molecule. It is known that ADAP plays a role in integrin-mediated signaling pathways leading to adhesion and motility in T lymphocytes. However, little is known about the role of ADAP in dendritic cells, a special cell population within the immune system linking the innate and the adaptive immunity. Using their long dendrites, these cells capture and process antigen material and present it to other immune cells. Here, we provide evidence that most dendritic cell functions are not affected by the lack of ADAP. Interestingly, ADAP-deficient dendritic cells showed defects in integrin-mediated cellular responses. These findings have important implications for the understanding of the role of ADAP in integrin-mediated signaling cascades in dendritic cells. This knowledge would also facilitate the therapeutic modulation of signal transd
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