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  • 1
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    Immunology. Memory T cells--local heroes in the struggle for immunity (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-03-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mackay, C R -- von Andrian, U H -- New York, N.Y. -- Science. 2001 Mar 23;291(5512):2323-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Arthritis and Asthma Program, Garvan Institute of Medical Research, Darlinghurst, NSW 2010, Australia. c.mackay@garvan.unsw.edu.au〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11269302" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/*immunology ; Antigens, Thy-1/immunology ; Antigens, Viral/immunology ; CD4-Positive T-Lymphocytes/*immunology ; CD8-Positive T-Lymphocytes/*immunology ; Cell Movement ; Humans ; *Immunologic Memory ; Lymphocyte Activation ; Lymphoid Tissue/*immunology ; Mice ; Receptors, CCR7 ; Receptors, Chemokine/metabolism ; Rhabdoviridae Infections/immunology ; T-Lymphocyte Subsets/*immunology ; Time Factors ; Vesicular stomatitis Indiana virus/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Immunology. T cell activation in six dimensions (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-06-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉von Andrian, Ulrich H -- New York, N.Y. -- Science. 2002 Jun 7;296(5574):1815-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Blood Research, Department of Pathology, Harvard Medical School, Boston, MA 02115, USA. uva@cbr.med.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12052942" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Animals ; Antigen Presentation ; Antigens/immunology ; Cell Movement ; Dendritic Cells/*immunology/physiology ; Lasers ; Lymph Nodes/*immunology ; *Lymphocyte Activation ; Mice ; Microscopy/methods ; Microscopy, Confocal/methods ; Microscopy, Fluorescence ; Organ Culture Techniques ; Ovalbumin/immunology ; Oxygen/physiology ; Receptors, Antigen, T-Cell/immunology ; T-Lymphocytes/cytology/*immunology/physiology ; T-Lymphocytes, Helper-Inducer/immunology/physiology ; Thymus Gland/cytology/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Subcapsular sinus macrophages prevent CNS invasion on peripheral infection with a neurotropic virus (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-06-26
    Description: Lymph nodes (LNs) capture microorganisms that breach the body's external barriers and enter draining lymphatics, limiting the systemic spread of pathogens. Recent work has shown that CD11b(+)CD169(+) macrophages, which populate the subcapsular sinus (SCS) of LNs, are critical for the clearance of viruses from the lymph and for initiating antiviral humoral immune responses. Here we show, using vesicular stomatitis virus (VSV), a relative of rabies virus transmitted by insect bites, that SCS macrophages perform a third vital function: they prevent lymph-borne neurotropic viruses from infecting the central nervous system (CNS). On local depletion of LN macrophages, about 60% of mice developed ascending paralysis and died 7-10 days after subcutaneous infection with a small dose of VSV, whereas macrophage-sufficient animals remained asymptomatic and cleared the virus. VSV gained access to the nervous system through peripheral nerves in macrophage-depleted LNs. In contrast, within macrophage-sufficient LNs VSV replicated preferentially in SCS macrophages but not in adjacent nerves. Removal of SCS macrophages did not compromise adaptive immune responses against VSV, but decreased type I interferon (IFN-I) production within infected LNs. VSV-infected macrophages recruited IFN-I-producing plasmacytoid dendritic cells to the SCS and in addition were a major source of IFN-I themselves. Experiments in bone marrow chimaeric mice revealed that IFN-I must act on both haematopoietic and stromal compartments, including the intranodal nerves, to prevent lethal infection with VSV. These results identify SCS macrophages as crucial gatekeepers to the CNS that prevent fatal viral invasion of the nervous system on peripheral infection.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2892812/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2892812/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Iannacone, Matteo -- Moseman, E Ashley -- Tonti, Elena -- Bosurgi, Lidia -- Junt, Tobias -- Henrickson, Sarah E -- Whelan, Sean P -- Guidotti, Luca G -- von Andrian, Ulrich H -- AI069259/AI/NIAID NIH HHS/ -- AI072252/AI/NIAID NIH HHS/ -- AI078897/AI/NIAID NIH HHS/ -- AR42689/AR/NIAMS NIH HHS/ -- P01 AI078897/AI/NIAID NIH HHS/ -- P01 AI078897-01/AI/NIAID NIH HHS/ -- P01 CA071932/CA/NCI NIH HHS/ -- P01 CA071932-12S29003/CA/NCI NIH HHS/ -- R01 AI069259/AI/NIAID NIH HHS/ -- R01 AI069259-06/AI/NIAID NIH HHS/ -- R01 AI072252/AI/NIAID NIH HHS/ -- R01 AI072252-04/AI/NIAID NIH HHS/ -- T32 GM007753/GM/NIGMS NIH HHS/ -- England -- Nature. 2010 Jun 24;465(7301):1079-83. doi: 10.1038/nature09118.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immune Disease Institute and Department of Pathology, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, Massachusetts 02115, USA. Matteo_Iannacone@hms.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20577213" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Central Nervous System/cytology/*immunology/*virology ; Dendritic Cells/immunology ; Injections ; Interferon Type I/immunology ; Lymph Nodes/cytology/*immunology/innervation/*virology ; Macrophages/*immunology/virology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Paralysis/complications/virology ; Peripheral Nerves/virology ; Receptor, Interferon alpha-beta/deficiency ; Rhabdoviridae Infections/complications/*immunology/virology ; Survival Rate ; Vesicular stomatitis Indiana virus/immunology/pathogenicity/physiology ; Vesicular stomatitis New Jersey virus/immunology/pathogenicity/physiology ; Vesiculovirus/*immunology/pathogenicity/physiology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 4
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    Dynamic visualization of thrombopoiesis within bone marrow (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-09-22
    Description: Platelets are generated from megakaryocytes (MKs) in mammalian bone marrow (BM) by mechanisms that remain poorly understood. Here we describe the use of multiphoton intravital microscopy in intact BM to visualize platelet generation in mice. MKs were observed as sessile cells that extended dynamic proplatelet-like protrusions into microvessels. These intravascular extensions appeared to be sheared from their transendothelial stems by flowing blood, resulting in the appearance of proplatelets in peripheral blood. In vitro, proplatelet production from differentiating MKs was enhanced by fluid shear. These results confirm the concept of proplatelet formation in vivo and are consistent with the possibility that blood flow-induced hydrodynamic shear stress is a biophysical determinant of thrombopoiesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Junt, Tobias -- Schulze, Harald -- Chen, Zhao -- Massberg, Steffen -- Goerge, Tobias -- Krueger, Andreas -- Wagner, Denisa D -- Graf, Thomas -- Italiano, Joseph E Jr -- Shivdasani, Ramesh A -- von Andrian, Ulrich H -- HL068130/HL/NHLBI NIH HHS/ -- HL56949/HL/NHLBI NIH HHS/ -- HL63143/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2007 Sep 21;317(5845):1767-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immune Disease Institute and Department of Pathology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17885137" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Proteins ; Blood Platelets/*cytology ; Bone Marrow/*physiology ; Cells, Cultured ; Luminescent Proteins ; Megakaryocytes/*cytology ; Mice ; Microscopy, Fluorescence, Multiphoton ; Platelet Membrane Glycoprotein IIb ; Shear Strength ; Thrombopoiesis/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Generation of gut-homing IgA-secreting B cells by intestinal dendritic cells (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-11-18
    Description: Normal intestinal mucosa contains abundant immunoglobulin A (IgA)-secreting cells, which are generated from B cells in gut-associated lymphoid tissues (GALT). We show that dendritic cells (DC) from GALT induce T cell-independent expression of IgA and gut-homing receptors on B cells. GALT-DC-derived retinoic acid (RA) alone conferred gut tropism but could not promote IgA secretion. However, RA potently synergized with GALT-DC-derived interleukin-6 (IL-6) or IL-5 to induce IgA secretion. Consequently, mice deficient in the RA precursor vitamin A lacked IgA-secreting cells in the small intestine. Thus, GALT-DC shape mucosal immunity by modulating B cell migration and effector activity through synergistically acting mediators.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mora, J Rodrigo -- Iwata, Makoto -- Eksteen, Bertus -- Song, Si-Young -- Junt, Tobias -- Senman, Balimkiz -- Otipoby, Kevin L -- Yokota, Aya -- Takeuchi, Hajime -- Ricciardi-Castagnoli, Paola -- Rajewsky, Klaus -- Adams, David H -- von Andrian, Ulrich H -- AI-061663/AI/NIAID NIH HHS/ -- G0601816/Medical Research Council/United Kingdom -- HL54936/HL/NHLBI NIH HHS/ -- HL56949/HL/NHLBI NIH HHS/ -- HL62524/HL/NHLBI NIH HHS/ -- R37 AI054636/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2006 Nov 17;314(5802):1157-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉CBR Institute for Biomedical Research and Department of Pathology, Harvard Medical School, Boston, MA 02115, USA. mora@cbr.med.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17110582" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/*immunology/secretion ; Cell Movement ; Cells, Cultured ; Chemotaxis, Leukocyte ; Dendritic Cells/*immunology ; Immunity, Mucosal ; Immunoglobulin A/*biosynthesis/immunology ; Interleukin-5/immunology ; Interleukin-6/immunology ; Intestinal Mucosa/immunology ; Intestines/cytology/*immunology ; Lymphoid Tissue/cytology/immunology ; Mice ; Mice, Inbred C57BL ; Receptors, Antigen, B-Cell/biosynthesis ; Tretinoin/immunology ; Vitamin A/physiology ; Vitamin A Deficiency/immunology ; Vitamins/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    HIV-infected T cells are migratory vehicles for viral dissemination (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-08-03
    Description: After host entry through mucosal surfaces, human immunodeficiency virus-1 (HIV-1) disseminates to lymphoid tissues to establish a generalized infection of the immune system. The mechanisms by which this virus spreads among permissive target cells locally during the early stages of transmission and systemically during subsequent dissemination are not known. In vitro studies suggest that the formation of virological synapses during stable contacts between infected and uninfected T cells greatly increases the efficiency of viral transfer. It is unclear, however, whether T-cell contacts are sufficiently stable in vivo to allow for functional synapse formation under the conditions of perpetual cell motility in epithelial and lymphoid tissues. Here, using multiphoton intravital microscopy, we examine the dynamic behaviour of HIV-infected T cells in the lymph nodes of humanized mice. We find that most productively infected T cells migrate robustly, resulting in their even distribution throughout the lymph node cortex. A subset of infected cells formed multinucleated syncytia through HIV envelope-dependent cell fusion. Both uncoordinated motility of syncytia and adhesion to CD4(+) lymph node cells led to the formation of long membrane tethers, increasing cell lengths to up to ten times that of migrating uninfected T cells. Blocking the egress of migratory T cells from the lymph nodes into efferent lymph vessels, and thus interrupting T-cell recirculation, limited HIV dissemination and strongly reduced plasma viraemia. Thus, we have found that HIV-infected T cells are motile, form syncytia and establish tethering interactions that may facilitate cell-to-cell transmission through virological synapses. Migration of T cells in lymph nodes therefore spreads infection locally, whereas their recirculation through tissues is important for efficient systemic viral spread, suggesting new molecular targets to antagonize HIV infection.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3470742/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3470742/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Murooka, Thomas T -- Deruaz, Maud -- Marangoni, Francesco -- Vrbanac, Vladimir D -- Seung, Edward -- von Andrian, Ulrich H -- Tager, Andrew M -- Luster, Andrew D -- Mempel, Thorsten R -- P01 AI0178897/AI/NIAID NIH HHS/ -- P30 AI060354/AI/NIAID NIH HHS/ -- P30 AR042689/AR/NIAMS NIH HHS/ -- P30 DK043351/DK/NIDDK NIH HHS/ -- P30AI060354/AI/NIAID NIH HHS/ -- R01 CA150975/CA/NCI NIH HHS/ -- R56 AI097052/AI/NIAID NIH HHS/ -- T32 AI007387/AI/NIAID NIH HHS/ -- England -- Nature. 2012 Oct 11;490(7419):283-7. doi: 10.1038/nature11398. Epub 2012 Aug 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Center for Immunology and Inflammatory Diseases, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22854780" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CD4-Positive T-Lymphocytes/*virology ; Cell Movement ; Cells, Cultured ; Disease Models, Animal ; Female ; Giant Cells ; HIV/*immunology ; HIV Infections/*immunology/transmission/*virology ; Humans ; Lymph Nodes/virology ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Mice, Transgenic
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
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    Nociceptive sensory neurons drive interleukin-23-mediated psoriasiform skin inflammation (2014)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2014-04-25
    Description: The skin has a dual function as a barrier and a sensory interface between the body and the environment. To protect against invading pathogens, the skin harbours specialized immune cells, including dermal dendritic cells (DDCs) and interleukin (IL)-17-producing gammadelta T (gammadeltaT17) cells, the aberrant activation of which by IL-23 can provoke psoriasis-like inflammation. The skin is also innervated by a meshwork of peripheral nerves consisting of relatively sparse autonomic and abundant sensory fibres. Interactions between the autonomic nervous system and immune cells in lymphoid organs are known to contribute to systemic immunity, but how peripheral nerves regulate cutaneous immune responses remains unclear. We exposed the skin of mice to imiquimod, which induces IL-23-dependent psoriasis-like inflammation. Here we show that a subset of sensory neurons expressing the ion channels TRPV1 and Nav1.8 is essential to drive this inflammatory response. Imaging of intact skin revealed that a large fraction of DDCs, the principal source of IL-23, is in close contact with these nociceptors. Upon selective pharmacological or genetic ablation of nociceptors, DDCs failed to produce IL-23 in imiquimod-exposed skin. Consequently, the local production of IL-23-dependent inflammatory cytokines by dermal gammadeltaT17 cells and the subsequent recruitment of inflammatory cells to the skin were markedly reduced. Intradermal injection of IL-23 bypassed the requirement for nociceptor communication with DDCs and restored the inflammatory response. These findings indicate that TRPV1(+)Nav1.8(+) nociceptors, by interacting with DDCs, regulate the IL-23/IL-17 pathway and control cutaneous immune responses.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4127885/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4127885/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Riol-Blanco, Lorena -- Ordovas-Montanes, Jose -- Perro, Mario -- Naval, Elena -- Thiriot, Aude -- Alvarez, David -- Paust, Silke -- Wood, John N -- von Andrian, Ulrich H -- 101054/Wellcome Trust/United Kingdom -- 5F31AR063546-02/AR/NIAMS NIH HHS/ -- AI069259/AI/NIAID NIH HHS/ -- AI078897/AI/NIAID NIH HHS/ -- AI095261/AI/NIAID NIH HHS/ -- AI111595/AI/NIAID NIH HHS/ -- F31 AR063546/AR/NIAMS NIH HHS/ -- G0901905/Medical Research Council/United Kingdom -- P01 AI078897/AI/NIAID NIH HHS/ -- P01 AI112521/AI/NIAID NIH HHS/ -- R01 AI069259/AI/NIAID NIH HHS/ -- R01 AI111595/AI/NIAID NIH HHS/ -- England -- Nature. 2014 Jun 5;510(7503):157-61. doi: 10.1038/nature13199. Epub 2014 Apr 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Microbiology and Immunobiology, Harvard Medical School, Boston, Massachusetts 02115, USA [2]. ; Department of Microbiology and Immunobiology, Harvard Medical School, Boston, Massachusetts 02115, USA. ; 1] Department of Microbiology and Immunobiology, Harvard Medical School, Boston, Massachusetts 02115, USA [2] Department of Pediatrics, Baylor College of Medicine, Houston, Texas 77030, USA. ; Institute for Biomedical Research, University College London, London WC1E 6BT, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24759321" target="_blank"〉PubMed〈/a〉
    Keywords: Aminoquinolines ; Animals ; Disease Models, Animal ; Female ; Inflammation/chemically induced/immunology/pathology ; Interleukin-17/biosynthesis/immunology ; Interleukin-23/biosynthesis/*immunology ; Interleukins/biosynthesis/immunology ; Langerhans Cells/immunology/metabolism ; Lymph Nodes/immunology/pathology ; Male ; Mice ; Mice, Inbred C57BL ; NAV1.8 Voltage-Gated Sodium Channel/metabolism ; Nociceptors/drug effects/*metabolism ; Psoriasis/chemically induced/*immunology/*pathology ; Sensory Receptor Cells/drug effects/*metabolism ; Skin/cytology/immunology/*innervation/*pathology ; T-Lymphocytes/immunology/metabolism ; TRPV Cation Channels/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
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    Platelet-mediated lymphocyte delivery to high endothelial venules (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-07-12
    Description: Circulating lymphocytes gain access to lymph nodes owing to their ability to initiate rolling along specialized high endothelial venules (HEVs). One mechanism of rolling involves L-selectin binding to peripheral node addressin (PNAd) on HEVs. Activated platelets are shown to bind to circulating lymphocytes and to mediate rolling in HEVs, in vivo, through another molecule, P-selectin, which also interacts with PNAd. In vitro, activated platelets enhanced tethering of lymphocytes to PNAd and sustained lymphocyte rolling, even in the absence of functional L-selectin. Thus, a platelet pathway operating through P-selectin provides a second mechanism for lymphocyte delivery to HEVs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Diacovo, T G -- Puri, K D -- Warnock, R A -- Springer, T A -- von Andrian, U H -- HL48675/HL/NHLBI NIH HHS/ -- HL54936/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1996 Jul 12;273(5272):252-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Blood Research, Harvard Medical School, 200 Longwood Avenue, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8662511" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Surface/*metabolism ; Blood Platelets/*physiology ; Cell Adhesion ; Cell Movement ; Endothelium, Vascular/cytology ; Humans ; L-Selectin/physiology ; Ligands ; Lymph Nodes/*blood supply/cytology ; Lymphocytes/cytology/*physiology ; Membrane Glycoproteins/metabolism ; Membrane Proteins ; Mice ; P-Selectin/metabolism ; Platelet Activation ; Receptors, Lymphocyte Homing/metabolism ; Transfection ; Tumor Cells, Cultured ; Venules/cytology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    VACCINES. A mucosal vaccine against Chlamydia trachomatis generates two waves of protective memory T cells (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-06-20
    Description: Genital Chlamydia trachomatis (Ct) infection induces protective immunity that depends on interferon-gamma-producing CD4 T cells. By contrast, we report that mucosal exposure to ultraviolet light (UV)-inactivated Ct (UV-Ct) generated regulatory T cells that exacerbated subsequent Ct infection. We show that mucosal immunization with UV-Ct complexed with charge-switching synthetic adjuvant particles (cSAPs) elicited long-lived protection in conventional and humanized mice. UV-Ct-cSAP targeted immunogenic uterine CD11b(+)CD103(-) dendritic cells (DCs), whereas UV-Ct accumulated in tolerogenic CD11b(-)CD103(+) DCs. Regardless of vaccination route, UV-Ct-cSAP induced systemic memory T cells, but only mucosal vaccination induced effector T cells that rapidly seeded uterine mucosa with resident memory T cells (T(RM) cells). Optimal Ct clearance required both T(RM) seeding and subsequent infection-induced recruitment of circulating memory T cells. Thus, UV-Ct-cSAP vaccination generated two synergistic memory T cell subsets with distinct migratory properties.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4605428/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4605428/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stary, Georg -- Olive, Andrew -- Radovic-Moreno, Aleksandar F -- Gondek, David -- Alvarez, David -- Basto, Pamela A -- Perro, Mario -- Vrbanac, Vladimir D -- Tager, Andrew M -- Shi, Jinjun -- Yethon, Jeremy A -- Farokhzad, Omid C -- Langer, Robert -- Starnbach, Michael N -- von Andrian, Ulrich H -- 1 R01-EB015419-01/EB/NIBIB NIH HHS/ -- AI069259/AI/NIAID NIH HHS/ -- AI078897/AI/NIAID NIH HHS/ -- AI095261/AI/NIAID NIH HHS/ -- AI111595/AI/NIAID NIH HHS/ -- P01 AI078897/AI/NIAID NIH HHS/ -- P30-AI060354/AI/NIAID NIH HHS/ -- R00 CA160350/CA/NCI NIH HHS/ -- R01 AI039558/AI/NIAID NIH HHS/ -- R01 AI062827/AI/NIAID NIH HHS/ -- R01 AI069259/AI/NIAID NIH HHS/ -- R01 AI072252/AI/NIAID NIH HHS/ -- R01 AI111595/AI/NIAID NIH HHS/ -- R01 AI39558/AI/NIAID NIH HHS/ -- R37-EB000244/EB/NIBIB NIH HHS/ -- T32 HL066987/HL/NHLBI NIH HHS/ -- U19 AI095261/AI/NIAID NIH HHS/ -- U19 AI113187/AI/NIAID NIH HHS/ -- U54-CA119349/CA/NCI NIH HHS/ -- U54-CA151884/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2015 Jun 19;348(6241):aaa8205. doi: 10.1126/science.aaa8205.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Immunology, Department of Microbiology and Immunobiology, Harvard Medical School, Boston, MA 02115, USA. uva@hms.harvard.edu georg_stary@hms.harvard.edu. ; Division of Immunology, Department of Microbiology and Immunobiology, Harvard Medical School, Boston, MA 02115, USA. ; Harvard-MIT Division of Health Sciences and Technology, Cambridge, MA 02139, USA. Department of Chemical Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. ; Center for Immunology and Inflammatory Diseases, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA. ; Laboratory of Nanomedicine and Biomaterials, Department of Anesthesiology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. ; Sanofi Pasteur, Cambridge, MA 02139, USA. ; Laboratory of Nanomedicine and Biomaterials, Department of Anesthesiology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. King Abdulaziz University, Jeddah, Saudi Arabia. ; Division of Immunology, Department of Microbiology and Immunobiology, Harvard Medical School, Boston, MA 02115, USA. Ragon Institute of MGH, MIT and Harvard, Cambridge, MA 02139, USA. uva@hms.harvard.edu georg_stary@hms.harvard.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26089520" target="_blank"〉PubMed〈/a〉
    Keywords: Adjuvants, Immunologic/administration & dosage ; Animals ; Antigens, CD/immunology ; Antigens, CD11/immunology ; Bacterial Vaccines/administration & dosage/*immunology ; CD8-Positive T-Lymphocytes/immunology ; Chlamydia Infections/*prevention & control ; Chlamydia trachomatis/*immunology/radiation effects ; Dendritic Cells/immunology ; Female ; *Immunologic Memory ; Integrin alpha Chains/immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mucous Membrane/immunology ; Nanoparticles/administration & dosage ; T-Lymphocyte Subsets/immunology ; Th1 Cells/*immunology ; Ultraviolet Rays ; Uterus/*immunology ; Vaccination/methods ; Vaccines, Inactivated/administration & dosage/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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    SCS macrophages suppress melanoma by restricting tumor-derived vesicle-B cell interactions (2016)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2016-03-19
    Description: Tumor-derived extracellular vesicles (tEVs) are important signals in tumor-host cell communication, yet it remains unclear how endogenously produced tEVs affect the host in different areas of the body. We combined imaging and genetic analysis to track melanoma-derived vesicles at organismal, cellular, and molecular scales to show that endogenous tEVs efficiently disseminate via lymphatics and preferentially bind subcapsular sinus (SCS) CD169(+) macrophages in tumor-draining lymph nodes (tdLNs) in mice and humans. The CD169(+) macrophage layer physically blocks tEV dissemination but is undermined during tumor progression and by therapeutic agents. A disrupted SCS macrophage barrier enables tEVs to enter the lymph node cortex, interact with B cells, and foster tumor-promoting humoral immunity. Thus, CD169(+) macrophages may act as tumor suppressors by containing tEV spread and ensuing cancer-enhancing immunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pucci, Ferdinando -- Garris, Christopher -- Lai, Charles P -- Newton, Andita -- Pfirschke, Christina -- Engblom, Camilla -- Alvarez, David -- Sprachman, Melissa -- Evavold, Charles -- Magnuson, Angela -- von Andrian, Ulrich H -- Glatz, Katharina -- Breakefield, Xandra O -- Mempel, Thorsten R -- Weissleder, Ralph -- Pittet, Mikael J -- 1R01CA164448/CA/NCI NIH HHS/ -- 1R33CA202064/CA/NCI NIH HHS/ -- F31-CA196035/CA/NCI NIH HHS/ -- P01-CA069246/CA/NCI NIH HHS/ -- P50-CA86355/CA/NCI NIH HHS/ -- R01 AI097052/AI/NIAID NIH HHS/ -- R01-AI084880/AI/NIAID NIH HHS/ -- R01EB010011/EB/NIBIB NIH HHS/ -- R21-CA190344/CA/NCI NIH HHS/ -- T32CA79443/CA/NCI NIH HHS/ -- U19 CA179563/CA/NCI NIH HHS/ -- U54-CA126515/CA/NCI NIH HHS/ -- Canadian Institutes of Health Research/Canada -- New York, N.Y. -- Science. 2016 Apr 8;352(6282):242-6. doi: 10.1126/science.aaf1328. Epub 2016 Mar 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Systems Biology, Massachusetts General Hospital Research Institute, Harvard Medical School, Boston, MA 02114, USA. ; Center for Systems Biology, Massachusetts General Hospital Research Institute, Harvard Medical School, Boston, MA 02114, USA. Graduate Program in Immunology, Harvard Medical School, Boston, MA 02115, USA. ; Department of Neurology, Massachusetts General Hospital Research Institute, Harvard Medical School, Charlestown, MA 02129, USA. ; Department of Microbiology and Immunobiology, Harvard Medical School, Boston, MA 02115, USA. ; Institute of Pathology, University Hospital Basel, 4031 Basel, Switzerland. ; Center for Immunology and Inflammatory Diseases, Massachusetts General Hospital Research Institute, Harvard Medical School, Charlestown, MA 02129, USA. ; Center for Systems Biology, Massachusetts General Hospital Research Institute, Harvard Medical School, Boston, MA 02114, USA. mpittet@mgh.harvard.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26989197" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/*immunology/ultrastructure ; Cell Communication ; Extracellular Vesicles/*immunology ; Humans ; *Immune Tolerance ; Lymph Nodes/immunology ; Lymphatic Vessels/immunology ; Macrophages/chemistry/*immunology ; Melanoma/*immunology/pathology ; Melanoma, Experimental/immunology/pathology ; Mice ; Mice, Inbred C57BL ; Sialic Acid Binding Ig-like Lectin 1/analysis/immunology ; Skin Neoplasms/*immunology/pathology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
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