@misc{ArltSchwiebsJaptoketal.2014, author = {Arlt, Olga and Schwiebs, Anja and Japtok, Lukasz and Rueger, Katja and Katzy, Elisabeth and Kleuser, Burkhard and Radeke, Heinfried H.}, title = {Sphingosine-1-Phosphate modulates dendritic cell function: focus on non-migratory effects in vitro and in vivo}, series = {Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry and pharmacology}, volume = {34}, journal = {Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry and pharmacology}, number = {1}, publisher = {Karger}, address = {Basel}, issn = {1015-8987}, doi = {10.1159/000362982}, pages = {27 -- 44}, year = {2014}, abstract = {Dendritic cells (DCs) are the cutting edge in innate and adaptive immunity. The major functions of these antigen presenting cells are the capture, endosomal processing and presentation of antigens, providing them an exclusive ability to provoke adaptive immune responses and to induce and control tolerance. Immature DCs capture and process antigens, migrate towards secondary lymphoid organs where they present antigens to naive T cells in a well synchronized sequence of procedures referred to as maturation. Indeed, recent research indicated that sphingolipids are modulators of essential steps in DC homeostasis. It has been recognized that sphingolipids not only modulate the development of DC subtypes from precursor cells but also influence functional activities of DCs such as antigen capture, and cytokine profiling. Thus, it is not astonishing that sphingolipids and sphingolipid metabolism play a substantial role in inflammatory diseases that are modulated by DCs. Here we highlight the function of sphingosine 1-phosphate (S1P) on DC homeostasis and the role of SIP and SW metabolism in inflammatory diseases.}, language = {en} } @article{PieperMarekUnterbergetal.2014, author = {Pieper, Christian and Marek, Jasmin Jacqueline and Unterberg, Marlies and Schwerdtle, Tanja and Galla, Hans-Joachim}, title = {Brain capillary pericytes contribute to the immune defense in response to cytokines or LPS in vitro}, series = {Brain research : an international multidisciplinary journal devoted to fundamental research in the brain sciences}, volume = {1550}, journal = {Brain research : an international multidisciplinary journal devoted to fundamental research in the brain sciences}, publisher = {Elsevier}, address = {Amsterdam}, issn = {0006-8993}, doi = {10.1016/j.brainres.2014.01.004}, pages = {1 -- 8}, year = {2014}, abstract = {The prevention of an inflammation in the brain is one of the most important goals the body has to achieve. As pericytes are located on the abluminal side of the capillaries in the brain, their role in fighting against invading pathogens has been investigated in some points, mostly in their ability to behave like macrophages. Here we studied the potential of pericytes to react as immune cells under inflammatory conditions, especially regarding the expression of the inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), major histocompatibility complex II (MHC II) molecules, CD68, as well as the generation of reactive oxygen and nitrogen species (RONS), and their ability in phagocytosis. Quantitative real time PCR and western blot analysis showed that pericytes are able to increase the expression of typical inflammatory marker proteins after the stimulation with tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1 beta), interferon-gamma (IFN-gamma), or lipopolysaccharides (LPS). Depending on the different specific pro-inflammatory factors pericytes changed the expression of alpha smooth muscle actin (alpha SMA), the most predominant pericyte marker. We conclude that the role of the pericytes within the immune system is regulated and fine-tuned by different cytokines strongly depending on the time when the cytokines are released and their concentration. The present results will help to understand the pericyte mediated defense mechanisms in the brain.}, language = {en} }