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      Regulation of blood vascular permeability in the skin

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          Abstract

          Regulation of blood vessel permeability is essential for the homeostasis of peripheral tissues. This regulation controls the trafficking of plasma contents, including water, vitamins, ions, hormones, cytokines, amyloids, lipoproteins, carrier proteins, and immunoglobulins. The properties of blood vessels vary among tissues based on their structural differences: continuous, fenestrated, or sinusoidal. These three types of blood vessels have different charge and size barrier properties. The anionic luminal glycocalyx layer on endothelial cells establishes the “charge barrier” that repels the attachment of negatively charged blood cells and plasma molecules. In contrast, the “size barrier” of blood vessels largely relies on the interendothelial junctions (IEJs) between endothelial cells, which define the paracellular permeability. As in most peripheral tissues, blood capillaries in the skin are composed of continuous and/or fenestrated blood vessels that have relatively tighter IEJs compared to those in the internal organs. Small vesicles in the capillary endothelium were discovered in the 1950s, and studies have since confirmed that blood endothelial cells transport the plasma contents by endocytosis and subsequent transcytosis and exocytosis—this process is called transcellular permeability. The permeability of blood vessels is highly variable as a result of intrinsic and extrinsic factors. It is significantly elevated upon tissue inflammations as a result of disabled IEJs and increased paracellular permeability due to inflammatory mediators. An increase in transcellular permeability during inflammation has also been postulated. Here, we provide an overview of the general properties of vascular permeability based on our recent observations of murine skin inflammation models, and we discuss its physiological significance in peripheral homeostasis.

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          The blockade of immune checkpoints in cancer immunotherapy.

          Among the most promising approaches to activating therapeutic antitumour immunity is the blockade of immune checkpoints. Immune checkpoints refer to a plethora of inhibitory pathways hardwired into the immune system that are crucial for maintaining self-tolerance and modulating the duration and amplitude of physiological immune responses in peripheral tissues in order to minimize collateral tissue damage. It is now clear that tumours co-opt certain immune-checkpoint pathways as a major mechanism of immune resistance, particularly against T cells that are specific for tumour antigens. Because many of the immune checkpoints are initiated by ligand-receptor interactions, they can be readily blocked by antibodies or modulated by recombinant forms of ligands or receptors. Cytotoxic T-lymphocyte-associated antigen 4 (CTLA4) antibodies were the first of this class of immunotherapeutics to achieve US Food and Drug Administration (FDA) approval. Preliminary clinical findings with blockers of additional immune-checkpoint proteins, such as programmed cell death protein 1 (PD1), indicate broad and diverse opportunities to enhance antitumour immunity with the potential to produce durable clinical responses.
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            Regulated portals of entry into the cell.

            The plasma membrane is the interface between cells and their harsh environment. Uptake of nutrients and all communication among cells and between cells and their environment occurs through this interface. 'Endocytosis' encompasses several diverse mechanisms by which cells internalize macromolecules and particles into transport vesicles derived from the plasma membrane. It controls entry into the cell and has a crucial role in development, the immune response, neurotransmission, intercellular communication, signal transduction, and cellular and organismal homeostasis. As the complexity of molecular interactions governing endocytosis are revealed, it has become increasingly clear that it is tightly coordinated and coupled with overall cell physiology and thus, must be viewed in a broader context than simple vesicular trafficking.
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              Basement membranes: structure, assembly and role in tumour angiogenesis.

              In recent years, the basement membrane (BM)--a specialized form of extracellular matrix (ECM)--has been recognized as an important regulator of cell behaviour, rather than just a structural feature of tissues. The BM mediates tissue compartmentalization and sends signals to epithelial cells about the external microenvironment. The BM is also an important structural and functional component of blood vessels, constituting an extracellular microenvironment sensor for endothelial cells and pericytes. Vascular BM components have recently been found to be involved in the regulation of tumour angiogenesis, making them attractive candidate targets for potential cancer therapies.
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                Author and article information

                Contributors
                gyohei@kuhp.kyoto-u.ac.jp
                + 81-75-751-3605 , kaba@kuhp.kyoto-u.ac.jp
                Journal
                Inflamm Regen
                Inflamm Regen
                Inflammation and Regeneration
                BioMed Central (London )
                1880-9693
                1880-8190
                10 July 2017
                10 July 2017
                2017
                : 37
                : 11
                Affiliations
                [1 ]ISNI 0000 0004 0372 2033, GRID grid.258799.8, Department of Dermatology, , Kyoto University Graduate School of Medicine, ; 54 Shogoin-Kawahara, Sakyo, Kyoto, 606-8507 Japan
                [2 ]ISNI 0000 0004 0637 0221, GRID grid.185448.4, Singapore Immunology Network (SIgN) and Institute of Medical Biology, , Agency for Science, Technology and Research (A*STAR), ; Biopolis, Singapore
                [3 ]ISNI 0000 0004 1754 9200, GRID grid.419082.6, PRESTO, , Japan Science and Technology Agency, ; Saitama, Japan
                Article
                42
                10.1186/s41232-017-0042-9
                5725833
                29259710
                bad15609-ade1-41f5-b42b-c29bbb94b979
                © The Author(s) 2017

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 30 January 2017
                : 25 April 2017
                Funding
                Funded by: JSPS KAKENHI
                Award ID: 263395
                Award Recipient :
                Funded by: Grants-in-Aid for Scientific Research
                Award ID: 15H1155
                Award ID: 15K15417
                Award Recipient :
                Funded by: Japan Science and Technology Agency, Precursory Research for Embryonic Science and Technology
                Award ID: 16021031300
                Award Recipient :
                Funded by: FundRef http://dx.doi.org/10.13039/100009619, Japan Agency for Medical Research and Development;
                Award ID: 16ek0410011h0003
                Award ID: 16he0902003h0002
                Award Recipient :
                Categories
                Review
                Custom metadata
                © The Author(s) 2017

                blood vessel,permeability,interendothelial junctions,paracellular,transcellular,skin,inflammation,immunoglobulin

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