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Interferons (IFN) belong to the family of cytokines and have been described first in the late 1950s as an inhibitory factor of viral replication. Since then, the impact of interferon has been greatly expanded and its function comprises a role not only in different types of infection, cancer and autoimmunity but importantly also in immunehomeostasis. IFN have important anti-viral effects but it is becoming more and more evident that they are true immunomodulators and have an important impact on the development and maintenance of innate and adaptive immunity.
interferons --- IFN --- immunehomeostasis --- autoimmunity --- mmunomodulators
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Interferons (IFN) belong to the family of cytokines and have been described first in the late 1950s as an inhibitory factor of viral replication. Since then, the impact of interferon has been greatly expanded and its function comprises a role not only in different types of infection, cancer and autoimmunity but importantly also in immunehomeostasis. IFN have important anti-viral effects but it is becoming more and more evident that they are true immunomodulators and have an important impact on the development and maintenance of innate and adaptive immunity.
Medicine --- Immunology --- interferons --- IFN --- immunehomeostasis --- autoimmunity --- mmunomodulators
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Interferons (IFN) belong to the family of cytokines and have been described first in the late 1950s as an inhibitory factor of viral replication. Since then, the impact of interferon has been greatly expanded and its function comprises a role not only in different types of infection, cancer and autoimmunity but importantly also in immunehomeostasis. IFN have important anti-viral effects but it is becoming more and more evident that they are true immunomodulators and have an important impact on the development and maintenance of innate and adaptive immunity.
Medicine --- Immunology --- interferons --- IFN --- immunehomeostasis --- autoimmunity --- mmunomodulators
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Successful containment of an infection is dependent on both innate and adaptive immune response. Cytokines are essential effectors of both of these systems. In particular, type I interferons (IFN-I) are important components of early innate immunity against an infection. However, the production of IFN-I could serve as a double edge sword, either containing an infection or enhancing susceptibility. For example, IFN-I, which is essential for early containment of viral infections, has been shown to be detrimental to the host during bacterial infections. In fact, recent significant reports have shown that influenza virus induced IFN-I responses can enhance the host susceptibility to secondary bacterial infections. These recent reports highlight the expanding immunoregulatory role of IFN-I in the host immunity. With these recent findings in mind, the aim of this research topic is to welcome novel data, opinion and literature reviews on the newly identified dual functions of IFN-I. This research topic wills focus on the following areas of IFN-I: 1) a detrimental role of IFN-I during primary bacterial infection; 2) a detrimental role of viral infection induced IFN-I during secondary bacterial infections; 3) evolutionary pressure that drove detrimental IFN-I response during primary bacterial infection; and 4) does benefit of IFN-I responses during primary viral infections outweigh the adverse consequences of IFN-I mediated enhanced susceptibility to secondary bacterial infections.
Autoimmunity --- adjuvant --- bacterial and viral infections --- Vaccine --- type I IFN
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Successful containment of an infection is dependent on both innate and adaptive immune response. Cytokines are essential effectors of both of these systems. In particular, type I interferons (IFN-I) are important components of early innate immunity against an infection. However, the production of IFN-I could serve as a double edge sword, either containing an infection or enhancing susceptibility. For example, IFN-I, which is essential for early containment of viral infections, has been shown to be detrimental to the host during bacterial infections. In fact, recent significant reports have shown that influenza virus induced IFN-I responses can enhance the host susceptibility to secondary bacterial infections. These recent reports highlight the expanding immunoregulatory role of IFN-I in the host immunity. With these recent findings in mind, the aim of this research topic is to welcome novel data, opinion and literature reviews on the newly identified dual functions of IFN-I. This research topic wills focus on the following areas of IFN-I: 1) a detrimental role of IFN-I during primary bacterial infection; 2) a detrimental role of viral infection induced IFN-I during secondary bacterial infections; 3) evolutionary pressure that drove detrimental IFN-I response during primary bacterial infection; and 4) does benefit of IFN-I responses during primary viral infections outweigh the adverse consequences of IFN-I mediated enhanced susceptibility to secondary bacterial infections.
Autoimmunity --- adjuvant --- bacterial and viral infections --- Vaccine --- type I IFN
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Successful containment of an infection is dependent on both innate and adaptive immune response. Cytokines are essential effectors of both of these systems. In particular, type I interferons (IFN-I) are important components of early innate immunity against an infection. However, the production of IFN-I could serve as a double edge sword, either containing an infection or enhancing susceptibility. For example, IFN-I, which is essential for early containment of viral infections, has been shown to be detrimental to the host during bacterial infections. In fact, recent significant reports have shown that influenza virus induced IFN-I responses can enhance the host susceptibility to secondary bacterial infections. These recent reports highlight the expanding immunoregulatory role of IFN-I in the host immunity. With these recent findings in mind, the aim of this research topic is to welcome novel data, opinion and literature reviews on the newly identified dual functions of IFN-I. This research topic wills focus on the following areas of IFN-I: 1) a detrimental role of IFN-I during primary bacterial infection; 2) a detrimental role of viral infection induced IFN-I during secondary bacterial infections; 3) evolutionary pressure that drove detrimental IFN-I response during primary bacterial infection; and 4) does benefit of IFN-I responses during primary viral infections outweigh the adverse consequences of IFN-I mediated enhanced susceptibility to secondary bacterial infections.
Autoimmunity --- adjuvant --- bacterial and viral infections --- Vaccine --- type I IFN
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This eBook is a collection of articles from a Frontiers Research Topic. Frontiers Research Topics are very popular trademarks of the Frontiers Journals Series: they are collections of at least ten articles, all centered on a particular subject. With their unique mix of varied contributions from Original Research to Review Articles, Frontiers Research Topics unify the most influential researchers, the latest key findings and historical advances in a hot research area! Find out more on how to host your own Frontiers Research Topic or contribute to one as an author by contacting the Frontiers Editorial Office: frontiersin.org/about/contact
interferon --- type III IFNs --- barrier --- inflammation --- IFN lambda
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Endocrine and immune parameters, namely glucocorticoid receptors (GcR) and IFN-gamma production in peripheral blood mononuclear cells (PBMC), and corticosterone in plasma, were studied in groups of four male rabbits observed in seminatural conditions in relation to agonistic behaviour and to seasonal variations. These parameters were selected on the basis of the findings that the presence of GcR in PBMC gives an indication of the in vivo biological effects of glucocorticoids and that PBMC cytokine production and plasma corticosterone are related to social behaviour. The frequency of active and passive behaviours was used to rank the animals. Seasonal variations were present for agonistic behaviours (Attack, Follow, Chase) and For plasma corticosterone, which were significantly higher in winter. IFN-gamma production in PBMC was increased after social interactions in both seasons, while plasma corticosterone was increased only in winter: GcR capacity in PBMC was decreased after social interactions. The results indicate that social and physical environmental factors are correlated with immune-endocrine functions
Agonistic behaviour,seasonal variation,corticosterone,glucocorticoid receptors,ifn-gamma production,rabbit. --- Agonistic behaviour. --- Agonistic. --- Animal. --- Animals. --- Behavior. --- Behaviour. --- Blood mononuclear-cells. --- Blood. --- Corticosterone. --- Dominance. --- Endocrine. --- Frequency. --- Function. --- Glucocorticoid receptors. --- Glucocorticoid. --- Glucocorticoids. --- Group. --- Hippocampal electrical-activity. --- Immune. --- Interaction. --- Interactions. --- Invivo. --- Male. --- Parameters. --- Physical. --- Pituitary. --- Plasma corticosterone. --- Plasma-corticosterone. --- Plasma. --- Production. --- Rabbit. --- Rabbits. --- Rank. --- Receptor. --- Receptors. --- Release. --- Responses. --- Season. --- Seasonal variation. --- Social behaviour. --- Social interaction. --- Social interactions. --- Social-interaction. --- Social. --- Stress. --- Variation.
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Rheumatoid Arthritis (RA) is a chronic inflammatory disease leading to joint inflammation and destruction. Treatment of RA includes the use of conventional (cs), biologic (b) disease-modifying anti-rheumatic drugs (DMARDs), and oral or intraarticular (IA) glucocorticoids (GCs). All different classes of drugs have shown to halt disease progression in clinical studies. In real life, a physician has more options than just adding or switching to a new ts/bDMARD if any kind of DMARDs has failed. They can modify or optimize the therapy with concomitant csDMARDs, and oral or IA-GC can be added to the treatment regimen. The EULAR states that therapeutic adjustment including the "optimization of csDMARDs dose or route of administration or intra-articular injections of GCs" is recommended. Thus, a new therapeutic agent can be embedded in a whole strategy with parallel optimization of the csDMARD and GC treatment. The idea of treating to target (T2T) for the treatment of RA patients has been around since the late 1990s. Many clinical studies (Ticora, BsSt, Camera) have demonstrated the superiority of a T2T approach. When I talk to physicians, I understand that most of them only rarely inject joints with GC. Therefore, I would like to create an issue on the T2T approach in reality including primary data, reviews, and real-life data demonstrating the general opinion and execution of T2T in treating RA.
Medicine --- rheumatoid arthritis --- sleep --- sleep disorders --- pain --- osteoporosis --- fracture --- fracture risk assessment tool --- treat-to-target --- certolizumab pegol --- csDMARDs --- glucocorticoids --- intra-articular injections --- DAS 28 --- ACR response --- HAQ-DI --- TNFα --- golimumab --- efficacy --- tolerability --- immunogenicity --- methotrexate --- posology --- titration --- oral route --- subcutaneous route --- bioavailability --- effectiveness --- periodontitis --- periodontal disease --- anti-citrullinated protein autoantibodies --- rheumatoid factor --- smoking --- medication --- Porphyromonas gingivalis --- Rheumatoid arthritis --- matrix metalloproteinase 3 --- infliximab --- pharmacogenomics --- anti-TNF --- personalized medicine --- baricitinib --- disease-modifying antirheumatic drugs --- pain perception --- outcomes research --- patient perspective --- Rheumatoid Arthritis --- therapy --- DMARD --- MTX --- Tumor Necrosis Factor-Alpha Inhibitors --- ankylosing spondylitis --- biosimilar --- switching --- synovial fibroblasts --- cytokine --- osteoclast --- herbal medicine --- methylation --- next-generation sequencing --- recovery of function --- fatigue --- productivity --- tofacitinib --- oral --- Th1.17 --- IL-17A --- IFN-γ, CD73 --- adenosine --- psoriatic arthritis --- regulation --- pseudoerosions --- hand --- foot --- ultrasonography --- radiography --- computed tomography --- magnetic resonance imaging --- n/a
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The regenerative and immunomodulatory properties of mesenchymal stem cells (MSCs) have made these cells the focus of multiple pre-clinical studies and clinical trials. While the results from these clinical studies have established that MSCs are safe, the efficacy of these cells is not as well-established. In this regard, there have been increased efforts towards generating potentiated/activated MSCs with enhanced therapeutic efficacy. Research on the mechanisms for enhancing MSC potency and efficacy is an area of active study with great potential for translation into clinical settings. The purpose of this book is to bring together recent research from a broad range of topics relating to potentiation strategies for enhancing MSC therapeutic efficacy, including growth factor pre-conditioning, hypoxia, and 3D culture. The research compiled in this book increases the basic understanding of MSC culture techniques and describes some MSC preparations for potential novel therapeutic applications.
Medicine --- cell therapy --- immunomodulation --- polyunsaturated fatty acid --- CD206 --- phagocytosis --- mesenchymal stem cells --- Vadadustat --- AKB-6548 --- preconditioning --- priming --- secretome --- chemotaxis --- Wharton’s jelly mesenchymal stem cells --- umbilical cord --- oxygen conditions --- secretory profile --- neuroprotection --- mesenchymal stromal cells --- 3D culture --- neurospheres --- spheroids --- pluripotency --- neural --- quiescence --- mesothelioma --- malignant pleural mesothelioma (MPM) --- liver cirrhosis --- placenta-derived mesenchymal stem cells --- WKYMVm --- combination therapy --- iPSC-derived MSCs --- iMSC secretome --- pre-conditioning --- angiogenesis --- IFN-γ --- hypoxia --- potentiation of iMSC efficacy --- nanofiber-hydrogel composite --- spinal cord injury --- inflammation --- macrophages --- secondary injury --- astrocytes --- axon growth --- adipose tissue-derived stem cells (ASCs) --- autophagy --- rapamycin --- 3-methyladenine --- immunosuppression --- exosome --- engineered cardiac patches --- adipose-derived stem cell --- paracrine potential --- osteogenic differentiation --- hepatocyte growth factor --- fibroblast growth factor 2
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