In this paper we present a physically-based model aimed at calculating the Photon Detection Efficiency (PDE) and the\ud temporal response of a Single-Photon Avalanche Diode (SPAD) with a given structure. In order to calculate these quantities, it is necessary to evaluate both the probability and the delay with which a photon impinging on the detector area triggers an avalanche. Three tasks are sequentially performed: as a first step, the electron-hole generation profile along the device is calculated according to the silicon absorption coefficient at the considered wavelength; successively, temporal evolution of the carriers distribution along the device is calculated by solving drift diffusion equations; finally, the avalanche triggering probability is calculated as a function of the photon absorption point.\ud Validation of the model has been carried out by comparing simulation and experimental results of a few generations of detectors previously realized in our laboratory. Photon detection efficiency has been measured and calculated for wavelengths ranging from 400nm to 1000nm and for excess bias voltages ranging from 2 to 8V. Similarly, temporal response has been investigated at two different wavelengths (520 and 820nm). A remarkable agreement between experimental and simulation results has been obtained in the entire characterization domain simply starting from the measured doping profile and without the need of any fitting parameter. Consequently, we think that this model will be a valuable tool for the development of new detectors with improved performances

In vertebrates, microorganisms are recognized by pathogen recognition receptors (PRRs). Exposure of immune cells to the ligands of these receptors activates intracellular signaling cascades that rapidly induce the expression of a variety of genes. Within these genes, the cytokines family plays a crucial function because of its role in adaptive immunity induction and in tissue-specific functional regulation, such as tissue repair and tissue homeostasis during steady state conditions. Within the myeloid compartment, dendritic cells (DCs) release a variety of inflammatory cytokines in response to microbes. In this study, we show that BMDCs release IL-22 directly upon PRRs activation without the need of IL-23 signaling as reported for other IL22-producing cells. Moreover, we demonstrate that cytokine IL-22 is rapidly released in a cell-specific manner as macrophages are not able to produce IL-22 through the same PRRs system. In addition, we characterize the intracellular signaling cascade required for IL-22 release in BMDCs. Myd88, MEK1/2, NFkb and AhR, but not p38, NFAT, and RORgt, were found to be involved in IL-22 regulation in DCs. Our study suggests that BMDCs possess a unique intracellular molecular plasticity which, once activated, directs different BMDCs functions in a cell-specific manner.

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