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The PI3Ks control many key functions in immune cells. PI3Ks phosphorylate PtdIns(4,5)P2 to yield PtdIns(3,4,5)P3. Initially, PI3K inhibitors such as Wortmannin, LY294002 and Rapamycin were used to establish a central role for Pi3K pathway in immune cells. Considerable progress in understanding the role of this pathway in cells of the immune system has been made in recent years, starting with analysis of various PI3K and Pten knockout mice and subsequently mTOR and Foxo knockout mice. Together, these experiments have revealed how PI3Ks control B cell and T cell development, T helper cell differentiation, regulatory T cell development and function, B cell and T cell trafficking, immunoglobulin class switching and much, much more. The PI3Kd inhibitor idelalisib has recently been approved for the treatment of B cell lymphoma. Clinical trials of other PI3K inhibitors in autoimmune and inflammatory diseases are also in progress. This is an opportune time to consider a Research Topic considering when what we have learned about the PI3K signalling module in lymphocyte biology and how this is making an impact on clinical immunology and haematology.

Immunologic diseases. --- B cell --- PI3K/AKT/mTOR --- Signal Transduction --- T cell --- PI3K pathway inhibitors

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Strong evidence continues to accumulate indicating that amyloid-beta (Aβ) is a central part of Alzheimer’s disease (AD) pathogenesis in spite of the negative evidence coming from failed clinical trials. Therefore, mechanisms of clearance of Aβ are of great interest in understanding AD pathogenesis and the development of effective treatments. This topic focuses on the issues related to Aβ clearance in AD. The topics covered include proteases that degrade Aβ and their localization, regulation, and functions. This topic also covers issues related to clearance through uptake by glia and through low-density lipoprotein (LDL) receptor mediated mechanisms. Signal transduction related to AD pathology and clearance is also addressed. Finally, immunotherapy and other novel therapeutic approaches are discussed.

Alzheimer's disease. --- Alzheimer's disease --- Alzheimer's disease --- Neurosciences. --- amyloid-beta --- Signal Transduction --- Proteases --- LDL receptors --- Clearance --- Alzheimer's disease --- Pathogenesis. --- Molecular aspects. --- amyloid-beta --- Signal Transduction --- Proteases --- LDL receptors --- Clearance --- Alzheimer's disease

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Arrest chemokines are a small group of chemokines that promote leukocyte arrest from rolling by triggering rapid integrin activation. Arrest chemokines have been described for neutrophils, monocytes, eosinophils, naïve lymphocytes and effector memory T cells. Most arrest chemokines are immobilized on the endothelial surface by binding to heparan sulfate proteoglycans. Whether soluble chemokines can promote integrin activation and arrest is controversial. Many aspects of the signaling pathway from the GPCR chemokine receptor to integrin activation are the subject of active investigation. Leukocyte adhesion deficiency III is a human disease in which chemokine-triggered integrin activation is defective because of a mutation in the cytoskeletal protein kindlin-3. About 10 different such mutations have been described. The defects seen in patients with LAD-III elucidate the importance of rapid integrin activation for host defense in humans. Here we present a series of ten reports that help clarify this crucial first step in the process of leukocyte transendothelial migration.

Chemokines --- Immunologic diseases. --- Immunology. --- chemokine --- LFA-1 --- Signal Transduction --- Talin --- integrin --- leukocyte adhesion --- VLA-4 --- Kindlin-3

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This book surveys healthy and diseased vascular systems in a multitude of model organisms and systems. It explores a plethora of functions, characteristics, and pathologies of the vascular system such as angiogenesis, fibroblast growth factor signaling, lymphangiogenesis, junctional signaling, the extracellular matrix, vascular permeability, leukocyte extravasation, axon guidance factors, the angiopoietin system, and chronic obstructive lung disease. Following a preface from leading researcher Dr. Holger Gerhardt, the text is divided into three sections- the first examining the development of the vascular system in a variety of contexts, the second delving into its homeostatic characteristics, and the third discussing its pathophysiologies.  The sixteen chapters, which represent international clinical and research perspectives, highlight the importance of molecular and signaling pathways for translational basic science and clinical medicine. Additionally, the text explores new and exciting fields in vascular biology research.   Comprehensive in both content and approach, Vascular Signaling in Health and Disease is ideal for graduate students, researchers, and clinicians interested in vascular biology, pneumology, and molecular biology.

Cellular signal transduction --- Endothelial cells --- Endothelial Cells --- Signal Transduction --- Biochemical Processes --- Epithelial Cells --- Cells --- Biochemical Phenomena --- Anatomy --- Chemical Phenomena --- Phenomena and Processes --- Physiology --- Human Anatomy & Physiology --- Health & Biological Sciences --- Cellular signal transduction. --- Endothelial cells. --- Endotheliocytes --- Cellular information transduction --- Information transduction, Cellular --- Signal transduction, Cellular --- Medicine. --- Human physiology. --- Angiology. --- Hematology. --- Systems biology. --- Cell physiology. --- Biomedicine. --- Human Physiology. --- Cell Physiology. --- Systems Biology. --- Epithelial cells --- Bioenergetics --- Cellular control mechanisms --- Information theory in biology --- Angiography. --- Biological models. --- Models, Biological --- Blood-vessels --- Diagnosis, Radioscopic --- Radiography, Medical --- Haematology --- Internal medicine --- Blood --- Cell function --- Cytology --- Human biology --- Medical sciences --- Human body --- Radiography --- Diseases --- Computational biology --- Bioinformatics --- Biological systems --- Molecular biology

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Strong evidence continues to accumulate indicating that amyloid-beta (Aβ) is a central part of Alzheimer’s disease (AD) pathogenesis in spite of the negative evidence coming from failed clinical trials. Therefore, mechanisms of clearance of Aβ are of great interest in understanding AD pathogenesis and the development of effective treatments. This topic focuses on the issues related to Aβ clearance in AD. The topics covered include proteases that degrade Aβ and their localization, regulation, and functions. This topic also covers issues related to clearance through uptake by glia and through low-density lipoprotein (LDL) receptor mediated mechanisms. Signal transduction related to AD pathology and clearance is also addressed. Finally, immunotherapy and other novel therapeutic approaches are discussed.

Alzheimer's disease. --- Alzheimer's disease --- Alzheimer's disease --- Neurosciences. --- Pathogenesis. --- Molecular aspects. --- amyloid-beta --- Signal Transduction --- Proteases --- LDL receptors --- Clearance --- Alzheimer's disease