The Experts below are selected from a list of 540501 Experts worldwide ranked by ideXlab platform
Carsten Claussen - One of the best experts on this subject based on the ideXlab platform.
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bone marrow mononuclear Cells activate angiogenesis via gap junction mediated Cell Cell Interaction
Stroke, 2020Co-Authors: Akie Kikuchitaura, Yuka Okinaka, Yukiko Takeuchi, Yuko Ogawa, Mitsuyo Maeda, Yosky Kataoka, Teruhito Yasui, Takafumi Kimura, Sheraz Gul, Carsten ClaussenAbstract:Background and Purpose- Bone marrow mononuclear Cells (BM-MNCs) are a rich source of hematopoietic stem Cells and have been widely used in experimental therapies for patients with ischemic diseases. Activation of angiogenesis is believed to be one of major BM-MNC mode of actions, but the essential mechanism by which BM-MNCs activate angiogenesis have hitherto been elusive. The objective of this study is to reveal the mechanism how BM-MNCs activate angiogenesis. Methods- We have evaluated the effect of direct Cell-Cell Interaction between BM-MNC and endothelial Cell on uptake of VEGF (vascular endothelial growth factor) into endothelial Cells in vitro. Cerebral ischemia model was used to evaluate the effects of direct Cell-Cell Interaction with transplanted BM-MNC on endothelial Cell at ischemic tissue. Results- The uptake of VEGF into endothelial Cells was increased by BM-MNC, while being inhibited by blockading the gap junction. Low-molecular-weight substance was transferred from BM-MNC into endothelial Cells via gap junctions in vivo, followed by increased expression of hypoxia-inducible factor-1α and suppression of autophagy in endothelial Cells. The concentration of glucose in BM-MNC cytoplasm was significantly higher than in endothelial Cells, and transfer of glucose homologue from BM-MNC to endothelial Cells was observed. Conclusions- Our findings demonstrated Cell-Cell Interaction via gap junction is the prominent pathway for activation of angiogenesis at endothelial Cells after ischemia and provided novel paradigm that energy source supply by stem Cell to injured Cell is one of the therapeutic mechanisms of Cell-based therapy. Visual Overview- An online visual overview is available for this article.
Ralf Bartenschlager - One of the best experts on this subject based on the ideXlab platform.
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revisiting dengue virus host Cell Interaction new insights into molecular and Cellular virology
Advances in Virus Research, 2014Co-Authors: Eliana G Acosta, Anil Kumar, Ralf BartenschlagerAbstract:Dengue virus (DENV) is an emerging mosquito-borne human pathogen that affects millions of individuals each year by causing severe and potentially fatal syndromes. Despite intense research efforts, no approved vaccine or antiviral therapy is yet available. Overcoming this limitation requires detailed understanding of the intimate relationship between the virus and its host Cell, providing the basis to devise optimal prophylactic and therapeutic treatment options. With the advent of novel high-throughput technologies including functional genomics, transcriptomics, proteomics, and lipidomics, new important insights into the DENV replication cycle and the Interaction of this virus with its host Cell have been obtained. In this chapter, we provide a comprehensive overview on the current status of the DENV research field, covering every step of the viral replication cycle with a particular focus on virus-host Cell Interaction. We will also review specific chemical inhibitors targeting Cellular factors and processes of relevance for the DENV replication cycle and their possible exploitation for the development of next generation antivirals.
Clayton Deming - One of the best experts on this subject based on the ideXlab platform.
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commensal dendritic Cell Interaction specifies a unique protective skin immune signature
Nature, 2015Co-Authors: Shruti Naik, Nicolas Bouladoux, Jonathan L Linehan, Seongji Han, Oliver J Harrison, Christoph Wilhelm, Sean Conlan, Sarah Himmelfarb, Allyson L Byrd, Clayton DemingAbstract:The skin represents the primary interface between the host and the environment. This organ is also home to trillions of microorganisms that play an important role in tissue homeostasis and local immunity. Skin microbial communities are highly diverse and can be remodelled over time or in response to environmental challenges. How, in the context of this complexity, individual commensal microorganisms may differentially modulate skin immunity and the consequences of these responses for tissue physiology remains unclear. Here we show that defined commensals dominantly affect skin immunity and identify the Cellular mediators involved in this specification. In particular, colonization with Staphylococcus epidermidis induces IL-17A(+) CD8(+) T Cells that home to the epidermis, enhance innate barrier immunity and limit pathogen invasion. Commensal-specific T-Cell responses result from the coordinated action of skin-resident dendritic Cell subsets and are not associated with inflammation, revealing that tissue-resident Cells are poised to sense and respond to alterations in microbial communities. This Interaction may represent an evolutionary means by which the skin immune system uses fluctuating commensal signals to calibrate barrier immunity and provide heterologous protection against invasive pathogens. These findings reveal that the skin immune landscape is a highly dynamic environment that can be rapidly and specifically remodelled by encounters with defined commensals, findings that have profound implications for our understanding of tissue-specific immunity and pathologies.
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commensal dendritic Cell Interaction specifies a unique protective skin immune signature
Nature, 2015Co-Authors: Shruti Naik, Nicolas Bouladoux, Jonathan L Linehan, Oliver J Harrison, Christoph Wilhelm, Sean Conlan, Sarah Himmelfarb, Allyson L Byrd, Clayton Deming, Mariam QuinonesAbstract:Defined skin commensal bacteria elicit a dermal dendritic-Cell-dependent, long-lasting, commensal-specific CD8+ T-Cell response that promotes protection against pathogens while preserving tissue homeostasis. The importance of our gut microbiota in health and disease is well established. Less clear is the role of the commensal microbes on the skin, where they interact with a tissue that, unlike the gut, is not designed for absorption. Here Yasmine Belkaid and colleagues examine the nature of the antigen presenting Cells involved in the dialogue between the immune system and skin commensals. They find that defined skin commensal bacteria elicit a dermal dendritic-Cell-dependent, long-lasting and commensal-specific CD8+ T-Cell response, while preserving tissue homeostasis. The CD8+ T Cells are shown to enhance innate protection against a fungal pathogen. The skin represents the primary interface between the host and the environment. This organ is also home to trillions of microorganisms that play an important role in tissue homeostasis and local immunity1,2,3,4. Skin microbial communities are highly diverse and can be remodelled over time or in response to environmental challenges5,6,7. How, in the context of this complexity, individual commensal microorganisms may differentially modulate skin immunity and the consequences of these responses for tissue physiology remains unclear. Here we show that defined commensals dominantly affect skin immunity and identify the Cellular mediators involved in this specification. In particular, colonization with Staphylococcus epidermidis induces IL-17A+ CD8+ T Cells that home to the epidermis, enhance innate barrier immunity and limit pathogen invasion. Commensal-specific T-Cell responses result from the coordinated action of skin-resident dendritic Cell subsets and are not associated with inflammation, revealing that tissue-resident Cells are poised to sense and respond to alterations in microbial communities. This Interaction may represent an evolutionary means by which the skin immune system uses fluctuating commensal signals to calibrate barrier immunity and provide heterologous protection against invasive pathogens. These findings reveal that the skin immune landscape is a highly dynamic environment that can be rapidly and specifically remodelled by encounters with defined commensals, findings that have profound implications for our understanding of tissue-specific immunity and pathologies.
B Furie - One of the best experts on this subject based on the ideXlab platform.
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platelet leukocyte endothelial Cell Interaction on the blood vessel wall
Seminars in Hematology, 1997Co-Authors: Alessandro Celi, Roberto Lorenzet, B FurieAbstract:Leukocytes, platelets, and endothelial Cells interact at sites of vascular injury and inflammation through adhesion receptors on the Cell surface. On binding of ligand to receptor, these receptors initiate intraCellular signaling that leads to the modulation of several biological properties of the Cells involved. These finely regulated processes involve several classes of Cell adhesion molecules: integrins, immunoglobulin-like proteins, selectins, and mucin-like proteins as well as an array of soluble mediators. Interaction of these Cell adhesion molecules serves to recruit circulating Cells to the blood vessel endothelium or to accumulated platelets on the vessel wall and to foster Cell-Cell communication. The importance of these Interactions to inflammation, blood coagulation, and the immune response is outlined.
Shruti Naik - One of the best experts on this subject based on the ideXlab platform.
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commensal dendritic Cell Interaction specifies a unique protective skin immune signature
Nature, 2015Co-Authors: Shruti Naik, Nicolas Bouladoux, Jonathan L Linehan, Seongji Han, Oliver J Harrison, Christoph Wilhelm, Sean Conlan, Sarah Himmelfarb, Allyson L Byrd, Clayton DemingAbstract:The skin represents the primary interface between the host and the environment. This organ is also home to trillions of microorganisms that play an important role in tissue homeostasis and local immunity. Skin microbial communities are highly diverse and can be remodelled over time or in response to environmental challenges. How, in the context of this complexity, individual commensal microorganisms may differentially modulate skin immunity and the consequences of these responses for tissue physiology remains unclear. Here we show that defined commensals dominantly affect skin immunity and identify the Cellular mediators involved in this specification. In particular, colonization with Staphylococcus epidermidis induces IL-17A(+) CD8(+) T Cells that home to the epidermis, enhance innate barrier immunity and limit pathogen invasion. Commensal-specific T-Cell responses result from the coordinated action of skin-resident dendritic Cell subsets and are not associated with inflammation, revealing that tissue-resident Cells are poised to sense and respond to alterations in microbial communities. This Interaction may represent an evolutionary means by which the skin immune system uses fluctuating commensal signals to calibrate barrier immunity and provide heterologous protection against invasive pathogens. These findings reveal that the skin immune landscape is a highly dynamic environment that can be rapidly and specifically remodelled by encounters with defined commensals, findings that have profound implications for our understanding of tissue-specific immunity and pathologies.
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commensal dendritic Cell Interaction specifies a unique protective skin immune signature
Nature, 2015Co-Authors: Shruti Naik, Nicolas Bouladoux, Jonathan L Linehan, Oliver J Harrison, Christoph Wilhelm, Sean Conlan, Sarah Himmelfarb, Allyson L Byrd, Clayton Deming, Mariam QuinonesAbstract:Defined skin commensal bacteria elicit a dermal dendritic-Cell-dependent, long-lasting, commensal-specific CD8+ T-Cell response that promotes protection against pathogens while preserving tissue homeostasis. The importance of our gut microbiota in health and disease is well established. Less clear is the role of the commensal microbes on the skin, where they interact with a tissue that, unlike the gut, is not designed for absorption. Here Yasmine Belkaid and colleagues examine the nature of the antigen presenting Cells involved in the dialogue between the immune system and skin commensals. They find that defined skin commensal bacteria elicit a dermal dendritic-Cell-dependent, long-lasting and commensal-specific CD8+ T-Cell response, while preserving tissue homeostasis. The CD8+ T Cells are shown to enhance innate protection against a fungal pathogen. The skin represents the primary interface between the host and the environment. This organ is also home to trillions of microorganisms that play an important role in tissue homeostasis and local immunity1,2,3,4. Skin microbial communities are highly diverse and can be remodelled over time or in response to environmental challenges5,6,7. How, in the context of this complexity, individual commensal microorganisms may differentially modulate skin immunity and the consequences of these responses for tissue physiology remains unclear. Here we show that defined commensals dominantly affect skin immunity and identify the Cellular mediators involved in this specification. In particular, colonization with Staphylococcus epidermidis induces IL-17A+ CD8+ T Cells that home to the epidermis, enhance innate barrier immunity and limit pathogen invasion. Commensal-specific T-Cell responses result from the coordinated action of skin-resident dendritic Cell subsets and are not associated with inflammation, revealing that tissue-resident Cells are poised to sense and respond to alterations in microbial communities. This Interaction may represent an evolutionary means by which the skin immune system uses fluctuating commensal signals to calibrate barrier immunity and provide heterologous protection against invasive pathogens. These findings reveal that the skin immune landscape is a highly dynamic environment that can be rapidly and specifically remodelled by encounters with defined commensals, findings that have profound implications for our understanding of tissue-specific immunity and pathologies.
