Artykuły w czasopismach na temat „Cytokine”
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Berti, E., i R. Caputo. "Cytokines, cytokine receptors and cytokine antibodies". Melanoma Research 6, SUPPLEMENT 1 (wrzesień 1996): S25. http://dx.doi.org/10.1097/00008390-199609001-00064.
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Trinchieri, Giorgio. "Cytokines and cytokine receptors". Immunological Reviews 202, nr 1 (grudzień 2004): 5–7. http://dx.doi.org/10.1111/j.0105-2896.2004.00217.x.
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Dayer, J. M. "Cytokines and cytokine antagonists". Fresenius' Journal of Analytical Chemistry 343, nr 1 (1992): 33–34. http://dx.doi.org/10.1007/bf00331973.
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van Deventer, S. J. H. "Cytokines and cytokine-based therapies". Current Opinion in Gastroenterology 14, nr 4 (lipiec 1998): 317–21. http://dx.doi.org/10.1097/00001574-199807000-00008.
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Li, Aileen W., i Wendell A. Lim. "Engineering cytokines and cytokine circuits". Science 370, nr 6520 (26.11.2020): 1034–35. http://dx.doi.org/10.1126/science.abb5607.
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Burger, D., i J. M. Dayer. "Inhibitory cytokines and cytokine inhibitors". Neurology 45, Issue 6, Supplement 6 (1.06.1995): S39—S43. http://dx.doi.org/10.1212/wnl.45.6_suppl_6.s39.
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Ansel, John, Patricia Perry, Jeffrey Brown, David Damm, Tuan Phan, Charles Hart, Thomas Luger i Stephen Hefeneider. "Cytokine Modulation of Keratinocyte Cytokines". Journal of Investigative Dermatology 94, nr 6 (czerwiec 1990): s101—s107. http://dx.doi.org/10.1111/1523-1747.ep12876053.
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Thipphawong, John. "Inhaled cytokines and cytokine antagonists". Advanced Drug Delivery Reviews 58, nr 9-10 (październik 2006): 1089–105. http://dx.doi.org/10.1016/j.addr.2006.07.014.
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Olbei, M., D. Modos, D. Cozzetto, N. Powell i T. Korcsmaros. "P070 Global cytokine—cytokine interaction framework to uncover communication channels between elements of the immune system". Journal of Crohn's and Colitis 17, Supplement_1 (30.01.2023): i236. http://dx.doi.org/10.1093/ecco-jcc/jjac190.0200.
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Abstract Background Cytokines are small peptides that signal between a variety of cell types and are one of the fundamental communication elements of the immune system. A variety of cytokine—cytokine interactions have previously been investigated in the literature, describing cytokines activating or inhibiting other cytokines in target cell types, and thus progressing the immune response to infection and illness. Disruption of cytokine communication is often an important goal in drug development as these compounds allow quelling and managing an overactive immune response in chronic diseases, such as Inflammatory Bowel Disease (IBD). In our previous work, we have introduced CytokineLink, a novel computational framework developed to establish cytokine—cytokine interactions from transcriptomics data (Olbei et al., Cells, 2021). Methods In this project, we generated a global network of cytokine—cytokine interactions based on cytokine response transcriptomics data from over 2000 datasets deposited in the CytoSig database. Using CytoSig’s significance analysis protocol, we established statistically significant cytokine—cytokine interactions, and determined the likely intracellular pathways connecting upstream and target cytokines using the OmniPath interaction resource. Results The resulting network is a signed, directed network of cytokine communication, containing 488 cytokine—cytokine interactions of 91 cytokines. The interactions in the network are annotated with the intracellular pathways that the included cytokines are anticipated to utilise, as well as the stimulatory and inhibitory effects that the cytokines have on one another. The resource captures the cytokine—cytokine networks of cytokines crucial in the pathophysiology of IBD, such as TNF, IL2, IL21, and OSM, which may grant novel insights into the cytokine pathways important in the molecular mechanisms underlying chronic diseases like IBD. The resource can be used by the community as a knowledge base for hypothesis generation, and is freely available through the NDEx platform. Conclusion In our work, we generated a novel computational framework collating how cytokines differentially regulate the expression of one another based on cytokine response transcriptomics data. The resulting interactions are signed, highlighting the inhibitory or stimulatory nature of the associations, and the change in expression associated with each link. The resource could be used to identify previously unknown network pharmacology targets, and to better understand the cytokine dysregulation in chronic diseases such as IBD by illustrating the interplay of the most influential IBD associated cytokines with other cytokines.
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Standiford, Theodore. "Anti-inflammatory Cytokines and Cytokine Antagonists". Current Pharmaceutical Design 6, nr 6 (1.04.2000): 633–49. http://dx.doi.org/10.2174/1381612003400533.
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BARRY, M., i G. McFADDEN. "Virus encoded cytokines and cytokine receptors". Parasitology 115, nr 7 (grudzień 1997): 89–100. http://dx.doi.org/10.1017/s0031182097001820.
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In order to replicate efficiently within the host, viruses have evolved multiple strategies to evade the host's immune system. In many cases viruses have actually hijacked various components of the host's immune system to ensure their own survival. One such strategy is the expression of virus encoded cytokines and cytokine receptors. Members of the poxvirus and herpesvirus families have been particularly successful with this strategy. The study of virus survival strategies provides important information regarding both virus biology as well as information about the immune system itself.
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Lin, Jian-Xin, i Warren J. Leonard. "Fine-Tuning Cytokine Signals". Annual Review of Immunology 37, nr 1 (26.04.2019): 295–324. http://dx.doi.org/10.1146/annurev-immunol-042718-041447.
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Cytokines are secreted or otherwise released polypeptide factors that exert autocrine and/or paracrine actions, with most cytokines acting in the immune and/or hematopoietic system. They are typically pleiotropic, controlling development, cell growth, survival, and/or differentiation. Correspondingly, cytokines are clinically important, and augmenting or attenuating cytokine signals can have deleterious or therapeutic effects. Besides physiological fine-tuning of cytokine signals, altering the nature or potency of the signal can be important in pathophysiological responses and can also provide novel therapeutic approaches. Here, we give an overview of cytokines, their signaling and actions, and the physiological mechanisms and pharmacologic strategies to fine-tune their actions. In particular, the differential utilization of STAT proteins by a single cytokine or by different cytokines and STAT dimerization versus tetramerization are physiological mechanisms of fine-tuning, whereas anticytokine and anticytokine receptor antibodies and cytokines with altered activities, including cytokine superagonists, partial agonists, and antagonists, represent new ways of fine-tuning cytokine signals.
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Olbei, M., J. Thomas, I. Hautefort, A. Treveil, B. Bohar, M. Madgwick, L. Gul, L. Csabai, D. Modos i T. Korcsmaros. "P090 Unraveling the rewiring of cytokine signalling in Inflammatory Bowel Disease using a novel network biology approach". Journal of Crohn's and Colitis 16, Supplement_1 (1.01.2022): i189. http://dx.doi.org/10.1093/ecco-jcc/jjab232.219.
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Abstract Background Intercellular communication mediated by cytokines is critical to the development of immune responses, particularly in the context of chronic immune-mediated disorders such as inflammatory bowel disease (IBD). By releasing these small molecular weight peptides, the source cells can influence numerous intracellular processes in the target cells, including the secretion of other cytokines downstream. However, there are no readily available resources and studies modelling cytokine-cytokine interactions that would be important for better understanding the dysregulation of cytokine signalling in IBD, and revealing potential new therapeutic targets for patients. Methods Based on the workflow of a cytokine signalling resource, CytokineLink, we developed previously, in this effort we built novel interaction networks using single-cell expression data from patients with ulcerative colitis (UC) and Crohn’s disease (CD). We defined two meta-networks for each disease: a cell–cell communication network connected by cytokines; and a cytokine–cytokine interaction network depicting the potential ways in which cytokines can affect the activity of each other. Results The rewiring of cell–cell and cytokine–cytokine interaction networks between healthy, non-inflamed and inflamed intestinal tissues in IBD was measured using the generated meta-networks. Cytokine-cytokine interaction networks revealed that in active UC, the Th1 cytokine IFNg and the chemokines CCL28 and CCL14 were central to cytokine-mediated communication networks. In CD, IL12B and IL13 formed the central cytokines in inflamed ileal tissues. Cell–cell interaction networks identified likely main cell types mediating the signalling of these key cytokines in non-inflamed and inflamed intestinal tissues: mast cells being the main source of IL13 in both IBD patients and healthy individuals. Conclusion We generated interaction networks aimed at capturing the most prevalent cell–cell and cytokine–cytokine interactions using disease specific single-cell expression data. Using the generated interaction networks we identified the condition-specific rewiring of cytokine mediated signalling in IBD, and key cytokines that could be targeted for ameliorating inflammatory responses. The data can be used by the community as a platform for hypothesis-generation. Potential use cases are deconvoluting the complexities of cytokine signalling in IBD to reveal potential cytokine drug targets, or predicting the downstream effects of drugs on cytokine responses.
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Zheng, Song, i Wu Wang. "Proinflammatory cytokine and cancer". American Journal of BioMedicine 4, nr 3 (11.07.2016): 240–55. http://dx.doi.org/10.18081/2333-5106/016-240-255.
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Many investigators have suggested that different cytokines may be important players in the development and progression of cancer and tumor biology. Cytokines are integral to many different aspects of cancer, including development/advancement, treatment, and prognosis. However, so far most cytokine -based therapy trials have fallen short of expectations. One of main obstacles is the difficulty to achieve therapeutically relevant dosage in patients without generating excessive normal tissue toxicity. Furthermore, cytokine profile levels have been used to predict cancer prognosis as differential cytokine expression profiles have been correlated with disease progression. Cytokines can also influence the effectiveness of cancer treatments. Elevated cytokine levels have been associated with reducing the anti-cancer activity of various treatments. In this review, we demonstrated the applicable action of cytokines in cancer pathogenesis and treatment.
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Lin, Sheng-Chieh, Li-Shian Shi i Yi-Ling Ye. "Advanced Molecular Knowledge of Therapeutic Drugs and Natural Products Focusing on Inflammatory Cytokines in Asthma". Cells 8, nr 7 (5.07.2019): 685. http://dx.doi.org/10.3390/cells8070685.
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Asthma is a common respiratory disease worldwide. Cytokines play a crucial role in the immune system and the inflammatory response to asthma. Abnormal cytokine expression may lead to the development of asthma, which may contribute to pathologies of this disease. As cytokines exhibit pleiotropy and redundancy characteristics, we summarized them according to their biologic activity in asthma development. We classified cytokines in three stages as follows: Group 1 cytokines for the epithelial environment stage, Group 2 cytokines for the Th2 polarization stage, and Group 3 cytokines for the tissue damage stage. The recent cytokine-targeting therapy for clinical use (anti-cytokine antibody/anti-cytokine receptor antibody) and traditional medicinal herbs (pure compounds, single herb, or natural formula) have been discussed in this review. Studies of the Group 2 anti-cytokine/anti-cytokine receptor therapies are more prominent than the studies of the other two groups. Anti-cytokine antibodies/anti-cytokine receptor antibodies for clinical use can be applied for patients who did not respond to standard treatments. For traditional medicinal herbs, anti-asthmatic bioactive compounds derived from medicinal herbs can be divided into five classes: alkaloids, flavonoids, glycosides, polyphenols, and terpenoids. However, the exact pathways targeted by these natural compounds need to be clarified. Using relevant knowledge to develop more comprehensive strategies may provide appropriate treatment for patients with asthma in the future.
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Makavchik, Svetlana A., Vladimir S. Avdeenko, Karina A. Moiseeva i Danil I. Safronov. "Laboratory methods for evaluating the functioning of cytokines in veterinary practice". Veterinariya, Zootekhniya i Biotekhnologiya 4, nr 125 (2024): 34–40. http://dx.doi.org/10.36871/vet.zoo.bio.202404004.
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This review paper analyzes modern laboratory methods for assessing the functioning of cytokines in veterinary practice for the prevention, prevention and development of treatment plans for pathologies of various etiologies. Purpose of the work: to analyze laboratory methods for assessing the functioning of cytokines in veterinary practice. Materials and methods. For the study, we used the resources of the Elibrary and PubMed search engines on this topic. Research results. A brief description of cytokines and their biological activity is presented. Laboratory methods for assessing the functioning of the cytokine system include: genetic analysis of mutations in the genes of cytokine receptors and proteins of intracellular signaling systems that trigger synthesis and signal transmission; analysis of cytokine gene polymorphism; study of cytokine gene expression; studying the level of cytokine production by cells in culture; determination of cytokine concentrations in biological fluids; study of cytokine synthesis at the level of individual cells; study of cytokine synthesis in tissues.
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Simbirtsev, A. S. "Immunopharmacological aspects of the cytokine system". Bulletin of Siberian Medicine 18, nr 1 (16.05.2019): 84–95. http://dx.doi.org/10.20538/1682-0363-2019-1-84-95.
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Cytokines represent a unique family of endogenous polypeptide mediators of intercellular interaction. From an immunopharmacological point of view cytokines can be marked out as a new, separate immunoregulatory molecule system and have some common biochemical properties and pleiotropic type of biological activity. In the cytokine regulatory system both reduction and elevation of cytokine levels can cause pathology. Several endogenous systems exist to control cytokine elevation and prevent tissue pathology. When synthesized simultaneously, cytokines form a cytokine chain. Deletion of any unit of this chain leads to the break in the formation of immunopathology. Cytokines as therapeutic preparations have evident advantages but also some limitations such as pharmacokinetics with short circulation period, adverse effects due to pleiotropic mode of action, and injectable drug forms. Rational design for clinical cytokine application could be linked with the development of prolonged and local drug forms or personalized cytokine therapy.
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Feliciani, C., A. K. Gupta i D. N. Saucier. "Keratinocytes and Cytokine/Growth Factors". Critical Reviews in Oral Biology & Medicine 7, nr 4 (październik 1996): 300–318. http://dx.doi.org/10.1177/10454411960070040101.
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Cytokines are polypeptide growth factors produced by most nucleated cells in the body, including epithelial cells, keratinocytes, and Langerhans cells in the skin. Cytokines can be classified into interleukins, tumor necrosis factors, chemokines, colony-stimulating factor, interferons, and growth factors. Like classic hormones, cytokines bind to specific receptors to transmit their messages to target cells. Cytokine receptors can be divided into three cytokine receptor superfamilies: the immunoglobulin superfamily, the hematopoietin family, and the tumor necrosis factor family. Following cytokine/cytokinereceptor binding (first messenger), a signal transduction pathway is initiated. Factors affecting homeostasis in the skin and oral mucosa include a delicate balance between cytokines/cytokine-receptors and their antagonists. An imbalance in these variables can influence the development of cutaneous and oral diseases—such as lichen planus, autoimmune disorders, and some neoplastic processes—and can affect wound healing. Potential uses of cytokines include cancer and antiviral therapy.
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Cui, Ang, Teddy Huang, Shuqiang Li, Aileen Ma, Jorge Perez, Derin Keskin, Chris Sander, Catherine J. Wu, Ernest Fraenkel i Nir Hacohen. "Systematic dissection of cytokine responses in vivo at single-cell resolution". Journal of Immunology 206, nr 1_Supplement (1.05.2021): 106.13. http://dx.doi.org/10.4049/jimmunol.206.supp.106.13.
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Abstract Cytokines mediate a highly complex intercellular signaling network in health and disease. While many individual cytokines have been studied in-depth, we do not have a systems-level view of cell-type-specific responses to each cytokine and do not yet understand how cytokines orchestrate cell-cell communication networks in a complex immune response. To address these two gaps in cytokine biology, we performed single-cell RNA sequencing to measure gene expression profiles of over 20 mouse lymph node cell populations in response to over 80 cytokines in vivo. We first investigated how distinct cell types respond to the same cytokine and found that while some pathways are activated across multiple cell types, many cytokines induced cell-type-specific gene expression signatures. Next, we compared responses across cytokines and found that cytokines induced both unique and shared biological processes. For example, in NK cells, we found that IL-2/7/12/15/27/33/36a, IFN-a1/b/g/e/k, LIF, CT-1, and NP each induced a cytolytic program, but also cytokine-specific gene expression programs involved in antigen presentation, NF-kB activation, and mRNA splicing. Finally, based on our compendium of cytokine signatures, we created an algorithm to assess the level of cytokine responses and reconstruct cell-cell communication networks, and used this approach to uncover cytokine mediators in checkpoint blockade cancer immunotherapy treatment. Our study provides a global view of cell-type specific cytokine responses in vivo. The framework can be readily applied to other transcriptomic datasets for assessing the roles of cytokines and cell-cell communication networks in any immune response.
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Drutskaya, M. S., E. O. Gubernatorova, E. A. Gorshkova, K. S. N. Athertkhany, M. A. Nosenko, V. S. Gogoleva, O. A. Namakanova, R. V. Zvartsev, A. A. Kruglov i S. A. Nedospasov. "Cytokines, reverse genetics and anti-cytokine therapy". Bulletin of Siberian Medicine 18, nr 1 (16.05.2019): 38–48. http://dx.doi.org/10.20538/1682-0363-2019-1-38-48.
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Cytokines comprise the molecular language of communication between the cells, which is needed to maintain the homeostatic functions of the body (including the immune system) and mediate various diseases. Many aspects of inflammation, autoimmune diseases and neoplasia are associated with cytokine signaling through specific receptors. The establishment of new physiological functions of “old” cytokines and understanding the molecular and cellular mechanisms of their involvement in disease pathogenesis, as well as the search for new therapeutic targets and development of innovative approaches to anti-cytokine therapy, present a fundamental problem. When assessing the tremendous success of anti-cytokine therapy in treatment of certain autoimmune diseases, we should not forget that (a) this treatment does not eliminate the causes of the disease:autoreactive T-cell clones; and that (b) less than half of the patients respond to this therapy; and that (c) anti-cytokine therapy has serious side effects.
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Kovanen, Panu E., i Warren J. Leonard. "Cytokine signaling: Inhibitors keep cytokines in check". Current Biology 9, nr 23 (grudzień 1999): R899—R902. http://dx.doi.org/10.1016/s0960-9822(00)80079-2.
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Nikovics, Krisztina, Anne-Laure Favier, Mathilde Rocher, Céline Mayinga, Johanna Gomez, Frédérique Dufour-Gaume i Diane Riccobono. "In Situ Identification of Both IL-4 and IL-10 Cytokine–Receptor Interactions during Tissue Regeneration". Cells 12, nr 11 (31.05.2023): 1522. http://dx.doi.org/10.3390/cells12111522.
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Cytokines secreted by individual immune cells regulate tissue regeneration and allow communication between various cell types. Cytokines bind to cognate receptors and trigger the healing process. Determining the orchestration of cytokine interactions with their receptors on their cellular targets is essential to fully understanding the process of inflammation and tissue regeneration. To this end, we have investigated the interactions of Interleukin-4 cytokine (IL-4)/Interleukin-4 cytokine receptor (IL-4R) and Interleukin-10 cytokine (IL-10)/Interleukin-10 cytokine receptor (IL-10R) using in situ Proximity Ligation Assays in a regenerative model of skin, muscle and lung tissues in the mini-pig. The pattern of protein–protein interactions was distinct for the two cytokines. IL-4 bound predominantly to receptors on macrophages and endothelial cells around the blood vessels while the target cells of IL-10 were mainly receptors on muscle cells. Our results show that in situ studies of cytokine–receptor interactions can unravel the fine details of the mechanism of action of cytokines.
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Olbei, Marton, John P. Thomas, Isabelle Hautefort, Agatha Treveil, Balazs Bohar, Matthew Madgwick, Lejla Gul, Luca Csabai, Dezso Modos i Tamas Korcsmaros. "CytokineLink: A Cytokine Communication Map to Analyse Immune Responses—Case Studies in Inflammatory Bowel Disease and COVID-19". Cells 10, nr 9 (29.08.2021): 2242. http://dx.doi.org/10.3390/cells10092242.
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Intercellular communication mediated by cytokines is critical to the development of immune responses, particularly in the context of infectious and inflammatory diseases. By releasing these small molecular weight peptides, the source cells can influence numerous intracellular processes in the target cells, including the secretion of other cytokines downstream. However, there are no readily available bioinformatic resources that can model cytokine–cytokine interactions. In this effort, we built a communication map between major tissues and blood cells that reveals how cytokine-mediated intercellular networks form during homeostatic conditions. We collated the most prevalent cytokines from the literature and assigned the proteins and their corresponding receptors to source tissue and blood cell types based on enriched consensus RNA-Seq data from the Human Protein Atlas database. To assign more confidence to the interactions, we integrated the literature information on cell–cytokine interactions from two systems of immunology databases, immuneXpresso and ImmunoGlobe. From the collated information, we defined two metanetworks: a cell–cell communication network connected by cytokines; and a cytokine–cytokine interaction network depicting the potential ways in which cytokines can affect the activity of each other. Using expression data from disease states, we then applied this resource to reveal perturbations in cytokine-mediated intercellular signalling in inflammatory and infectious diseases (ulcerative colitis and COVID-19, respectively). For ulcerative colitis, with CytokineLink, we demonstrated a significant rewiring of cytokine-mediated intercellular communication between non-inflamed and inflamed colonic tissues. For COVID-19, we were able to identify cell types and cytokine interactions following SARS-CoV-2 infection, highlighting important cytokine interactions that might contribute to severe illness in a subgroup of patients. Such findings have the potential to inform the development of novel, cytokine-targeted therapeutic strategies. CytokineLink is freely available for the scientific community through the NDEx platform and the project github repository.
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Ciampa, Maeghan L., Thomas A. O’Hara, Constance L. Joel, Melinda M. Gleaton, Kirti K. Tiwari, Daniel M. Boudreaux i Balakrishna M. Prasad. "Absence of “Cytokine Storm” in Hospitalized COVID-19 Patients: A Retrospective Cohort Study". Infectious Disease Reports 13, nr 2 (19.04.2021): 377–87. http://dx.doi.org/10.3390/idr13020036.
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Background: A rapidly growing number of publications cite “cytokine storm” as a contributing factor in coronavirus disease 2019 (COVID-19) pathology. However, a few recent reports led to questioning of “cytokine storm” theory in COVID-19. This study’s primary goal is to determine if exaggerated cytokine response in the range of a “cytokine storm” develops during the initial weeks of hospitalization in COVID-19 patients. Methods: Five proinflammatory cytokines reported to be involved in “cytokine storm” and elevated in COVID-19 (IL-6, IL-8, TNF-α, MCP-1, and IP-10) were analyzed in COVID-19, influenza (with “cytokine storm”: CS), and burn injury patients. The effect of dexamethasone use on cytokine response in COVID-19 was also analyzed. Results: None of the five cytokines in COVID-19 patients reached the lower threshold (95% CI) of the influenza (CS) group at any point during the study period. Furthermore, mean concentrations of all five cytokines in the influenza (CS) group and IL-6, IL-8, TNF-α in the burn group were significantly greater than in COVID-19 patients (p < 0.01). Dexamethasone treatment did not significantly alter the concentrations of any of the cytokines analyzed. Conclusions: Exaggerated cytokine response similar to “cytokine storm” was not observed in COVID-19 patients during two weeks of hospitalization.
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Melamud, Mark M., Evgeny A. Ermakov, Anastasiia S. Boiko, Daria A. Kamaeva, Alexey E. Sizikov, Svetlana A. Ivanova, Natalia M. Baulina, Olga O. Favorova, Georgy A. Nevinsky i Valentina N. Buneva. "Multiplex Analysis of Serum Cytokine Profiles in Systemic Lupus Erythematosus and Multiple Sclerosis". International Journal of Molecular Sciences 23, nr 22 (10.11.2022): 13829. http://dx.doi.org/10.3390/ijms232213829.
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Changes in cytokine profiles and cytokine networks are known to be a hallmark of autoimmune diseases, including systemic lupus erythematosus (SLE) and multiple sclerosis (MS). However, cytokine profiles research studies are usually based on the analysis of a small number of cytokines and give conflicting results. In this work, we analyzed cytokine profiles of 41 analytes in patients with SLE and MS compared with healthy donors using multiplex immunoassay. The SLE group included treated patients, while the MS patients were drug-free. Levels of 11 cytokines, IL-1b, IL-1RA, IL-6, IL-9, IL-10, IL-15, MCP-1/CCL2, Fractalkine/CX3CL1, MIP-1a/CCL3, MIP-1b/CCL4, and TNFa, were increased, but sCD40L, PDGF-AA, and MDC/CCL22 levels were decreased in SLE patients. Thus, changes in the cytokine profile in SLE have been associated with the dysregulation of interleukins, TNF superfamily members, and chemokines. In the case of MS, levels of 10 cytokines, sCD40L, CCL2, CCL3, CCL22, PDGF-AA, PDGF-AB/BB, EGF, IL-8, TGF-a, and VEGF, decreased significantly compared to the control group. Therefore, cytokine network dysregulation in MS is characterized by abnormal levels of growth factors and chemokines. Cross-disorder analysis of cytokine levels in MS and SLE showed significant differences between 22 cytokines. Protein interaction network analysis showed that all significantly altered cytokines in both SLE and MS are functionally interconnected. Thus, MS and SLE may be associated with impaired functional relationships in the cytokine network. A cytokine correlation networks analysis revealed changes in correlation clusters in SLE and MS. These data expand the understanding of abnormal regulatory interactions in cytokine profiles associated with autoimmune diseases.
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Łabędź, Wojciech, Anna Przybyla, Agnieszka Zimna, Mikołaj Dąbrowski i Łukasz Kubaszewski. "The Role of Cytokines in the Metastasis of Solid Tumors to the Spine: Systematic Review". International Journal of Molecular Sciences 24, nr 4 (14.02.2023): 3785. http://dx.doi.org/10.3390/ijms24043785.
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Although many studies have investigated the role of cytokines in bone metastases, our knowledge of their function in spine metastasis is limited. Therefore, we performed a systematic review to map the available evidence on the involvement of cytokines in spine metastasis in solid tumors. A PubMed search identified 211 articles demonstrating a functional link between cytokines/cytokine receptors and bone metastases, including six articles confirming the role of cytokines/cytokine receptors in spine metastases. A total of 68 cytokines/cytokine receptors were identified to mediate bone metastases; 9 (mostly chemokines) played a role in spine metastases: CXC motif chemokine ligand (CXCL) 5, CXCL12, CXC motif chemokine receptor (CXCR) 4, CXCR6, interleukin (IL) 10 in prostate cancer, CX3C motif chemokine ligand (CX3CL) 1 and CX3C motif chemokine receptor (CX3CR) 1 in liver cancer, CC motif chemokine ligand (CCL) 2 in breast cancer, and transforming growth factor (TGF) β in skin cancer. Except for CXCR6, all cytokines/cytokine receptors were shown to operate in the spine, with CX3CL1, CX3CR1, IL10, CCL2, CXCL12, and CXCR4 mediating bone marrow colonization, CXCL5 and TGFβ promoting tumor cell proliferation, and TGFβ additionally driving bone remodeling. The number of cytokines/cytokine receptors confirmed to mediate spinal metastasis is low compared with the vast spectrum of cytokines/cytokine receptors participating in other parts of the skeleton. Therefore, further research is needed, including validation of the role of cytokines mediating metastases to other bones, to precisely address the unmet clinical need associated with spine metastases.
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Olson, Matthew Richard, i Mark H. Kaplan. "Autocrine and paracrine cytokine feedback augment the production of Th2-associated cytokines." Journal of Immunology 196, nr 1_Supplement (1.05.2016): 191.22. http://dx.doi.org/10.4049/jimmunol.196.supp.191.22.
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Abstract The Type 2 cytokines (including cytokines from Th2 and Th9 cells) play a critical role in priming of the humoral response, immunity to parasites, and the induction of allergic disease. It has been proposed that unlike Type 1 cytokines (i.e. IFN-γ), the induction of Type 2 cytokines is cell autonomous and requires no additional signals for optimal cytokine production. Contrary to this notion, we found that the addition of golgi transport inhibitors that block cytokine secretion (i.e. monensin (Mon) and brefeldin A (BFA)) during stimulation significantly impaired the induction of Type 2, but not Type 1 cytokine mRNA and protein production. These data suggest that the release of cytokines by activated Th cells is uniquely required for further production of Type 2 cytokines. Mon and BFA strongly inhibited the release of IL-2 after stimulation and blockade of IL-2 during activation in the absence of golgi inhibitors significantly diminished Type 2 cytokine production. Further, transduction of cells with a constitutively active STAT5 negated the need for additional IL-2 signaling in driving Type 2 cytokine transcription, suggesting that STAT5 is the primary mediator of IL-2-driven gene expression. Interestingly, both autocrine and paracrine IL-2 production were capable of driving maximal Type 2 cytokine production. Taken together, these data indicate a novel role for IL-2 feedback in promoting Type 2 cytokine production and likely in promoting allergic inflammation.
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Hong, Chang-Sook, Brenda Diergaarde i Theresa L. Whiteside. "Abstract PO-096: Cytokines in the lumen of exosomes are undetectable by immunoassays distorting cytokine profiles in HNC patients and healthy donors". Clinical Cancer Research 29, nr 18_Supplement (15.09.2023): PO—096—PO—096. http://dx.doi.org/10.1158/1557-3265.aacrahns23-po-096.
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Abstract Background: Exosomes, now called small extracellular vesicles (sEV), play a key role in cell-to-cell signaling. They are produced by all cells, circulate freely and are present in all body fluids. Evidence indicates that biologically active cytokines are present on the surface and/or in the lumen of sEV. The contributions of intra-vesicular cytokines to cytokine levels in plasma of cancer patients are unknown. Methods: sEV were isolated by ultrafiltration/size exclusion chromatography from pre-cleared plasma obtained from 30 patients with head and neck squamous cell carcinoma (HNSCC) and 10 healthy donors (HDs). Multiplex immunoassays were used to measure cytokine levels in paired untreated and detergent treated (0.5% Triton X-100) plasma samples and in isolated detergent-treated sEV. Results: The presence of cytokines on the surface and lumen of sEV isolated from plasma of the patients and HDs was first confirmed by immunoblots and on-bead flow cytometry. sEV-associated cytokines were functional in various in vitro coincubation assays with responder immune or tissue cells. Using Ab microarrays for 80 cytokines, we showed that sEV from HNSCC plasma contained a greater variety of cytokines (71/80; 88.8%) than sEV of HDs (43/80; 53.8%). Patients’ sEV had higher cytokine levels (range p<0.01 to 0.05) than did sEV from HD’s plasma. A highly sensitive Curiox 65-plex platform was then used to compare cytokine levels in paired untreated and detergent-treated plasma of HNSCC patients. 51/65 (78.5%) cytokines in the panel were consistently detected in treated and untreated plasma, and the majority of these (45; 88.2%) were present at significantly higher levels (range p<0.0001-0.05) in detergent-treated plasma. The comparison of cytokine levels between treated plasma, untreated plasma and paired sEV showed that the observed differences were due to cytokines sequestered in sEV. The cytokines released from detergent-treated EVs significantly contributed to the incomplete overall cytokine profile of untreated plasma in HNSCC patients. Further, only cytokines in sEV or in detergent-treated plasma correlated with disease stage in HNSCC. Conclusions: In untreated patient plasma, multiplex immunoassays detected only soluble cytokines and missed cytokines contained in the sEV lumen. Permeabilization of sEV was necessary for the Ab-based detection of total plasma cytokines (i.e., soluble + sEV-bound). As sEV-associated cytokines are biologically active, their absence from the plasma cytokine profiles that are determined in untreated plasma leads to inaccurate cytokine measurements. Underestimated cytokine levels in disease likely contribute to the lack of clinically significant correlations of plasma cytokine levels with disease progression. Citation Format: Chang-Sook Hong, Brenda Diergaarde, Theresa L. Whiteside. Cytokines in the lumen of exosomes are undetectable by immunoassays distorting cytokine profiles in HNC patients and healthy donors [abstract]. In: Proceedings of the AACR-AHNS Head and Neck Cancer Conference: Innovating through Basic, Clinical, and Translational Research; 2023 Jul 7-8; Montreal, QC, Canada. Philadelphia (PA): AACR; Clin Cancer Res 2023;29(18_Suppl):Abstract nr PO-096.
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Liu, Yining, Min Zhao i Hong Qu. "Identification of cytokine-induced cell communications by pan-cancer meta-analysis". PeerJ 11 (1.12.2023): e16221. http://dx.doi.org/10.7717/peerj.16221.
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Cancer immune responses are complex cellular processes in which cytokine–receptor interactions play central roles in cancer development and response to therapy; dysregulated cytokine–receptor communication may lead to pathological processes, including cancer, autoimmune diseases, and cytokine storm; however, our knowledge regarding cytokine-mediated cell–cell communication (CCI) in different cancers remains limited. The present study presents a single-cell and pan-cancer-level transcriptomics integration of 41,900 cells across 25 cancer types. We developed a single-cell method to actively express 62 cytokine–receptor pairs to reveal stable cytokine-mediated cell communications involving 84 cytokines and receptors. The correlation between the sample-based CCI profile and the interactome analysis indicates multiple cytokine–receptor modules including TGFB1, IL16ST, IL15, and the PDGF family. Some isolated cytokine interactions, such as FN1–IL17RC, displayed diverse functions within over ten single-cell transcriptomics datasets. Further functional enrichment analysis revealed that the constructed cytokine–receptor interaction map is associated with the positive regulation of multiple immune response pathways. Using public TCGA pan-cancer mutational data, co-mutational analysis of the cytokines and receptors provided significant co-occurrence features, implying the existence of cooperative mechanisms. Analysis of 10,967 samples from 32 TCGA cancer types revealed that the 84 cytokine and receptor genes are significantly associated with clinical survival time. Interestingly, the tumor samples with mutations in any of the 84 cytokines and receptors have a substantially higher mutational burden, offering insights into antitumor immune regulation and response. Clinical cancer stage information revealed that tumor samples with mutations in any of the 84 cytokines and receptors stratify into earlier tumor stages, with unique cellular compositions and clinical outcomes. This study provides a comprehensive cytokine–receptor atlas of the cellular architecture in multiple cancers at the single-cell level.
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Minami, Keita, Yoshiki Yanagawa, Kazuya Iwabuchi, Nobuo Shinohara, Toru Harabayashi, Katsuya Nonomura i Kazunori Onoé. "Negative feedback regulation of T helper type 1 (Th1)/Th2 cytokine balance via dendritic cell and natural killer T cell interactions". Blood 106, nr 5 (1.09.2005): 1685–93. http://dx.doi.org/10.1182/blood-2004-12-4738.
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Abstract The ability of extracellular stimuli to modulate dendritic cell (DC) activation of natural killer T (NKT) cells was not well understood. We investigated the effects of the T helper type 1 (Th1)/Th2-cytokine environment on DC induction of NKT cell-mediated cytokine production in mice. Pretreatment of myeloid DCs with Th1 or Th2 cytokines, interleukin (IL)-4 or interferon (IFN)-γ, led to the enhanced production of reciprocal cytokines by NKT cells (eg, IL-4 pretreatment led to the enhanced production of Th1 cytokines) in vitro and in vivo. Thus, the recognition of Th1 or Th2 cytokines by DCs acts as a negative feedback loop to maintain Th1/Th2-cytokine balance via NKT cell functions. Using these data, we manipulated cytokine levels and innate cytolytic activity in vivo to increase an antitumor response. This is the first description of a novel regulation system governing Th1/Th2 cytokine balance involving DCs and NKT cells. (Blood. 2005;106:1685-1693)
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Tang, Xi-Dian, Tian-Tian Ji, Jia-Rui Dong, Hao Feng, Feng-Qiang Chen, Xi Chen, Hui-Ying Zhao, De-Kun Chen i Wen-Tao Ma. "Pathogenesis and Treatment of Cytokine Storm Induced by Infectious Diseases". International Journal of Molecular Sciences 22, nr 23 (30.11.2021): 13009. http://dx.doi.org/10.3390/ijms222313009.
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Cytokine storm is a phenomenon characterized by strong elevated circulating cytokines that most often occur after an overreactive immune system is activated by an acute systemic infection. A variety of cells participate in cytokine storm induction and progression, with profiles of cytokines released during cytokine storm varying from disease to disease. This review focuses on pathophysiological mechanisms underlying cytokine storm induction and progression induced by pathogenic invasive infectious diseases. Strategies for targeted treatment of various types of infection-induced cytokine storms are described from both host and pathogen perspectives. In summary, current studies indicate that cytokine storm-targeted therapies can effectively alleviate tissue damage while promoting the clearance of invading pathogens. Based on this premise, “multi-omics” immune system profiling should facilitate the development of more effective therapeutic strategies to alleviate cytokine storms caused by various diseases.
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Bonner, J. C., i A. R. Brody. "Cytokine-binding proteins in the lung". American Journal of Physiology-Lung Cellular and Molecular Physiology 268, nr 6 (1.06.1995): L869—L878. http://dx.doi.org/10.1152/ajplung.1995.268.6.l869.
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Numerous cytokines and growth factors signal the normal processes of tissue maintenance and remodeling in the lung, yet the aberrant expression of these peptide mediators is involved in a variety of pulmonary diseases. Furthermore, several different binding proteins function in controlling the extracellular levels of many of these cytokines in the lung. For example, a variety of cytokines and growth factors bind to and are regulated by the ubiquitous proteinase inhibitor, alpha 2-macroglobulin. The insulin-like growth factors are controlled by a specific class of six different insulin-like growth factor binding proteins. The transforming growth factor-beta family and fibroblast growth factors interact with extracellular matrix proteins. Several growth factor receptors are shed into the extracellular milieu where they retain a functional binding domain and thereby act as specific binding proteins. Cytokine-binding proteins appear to have a diversity of functions and may serve as extracellular cytokine reservoirs, protective shields against proteolytic degradation of cytokines, modifiers of cytokine-induced biological activity, or as clearance avenues for cytokines. The wide spectrum of cytokine-regulating molecules is important in cell-cell communications under normal conditions, whereas cytokine-binding protein dysfunction could contribute to a number of pulmonary diseases.
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Jansen, Joanneke E., Dominik Aschenbrenner, Holm H. Uhlig, Mark C. Coles i Eamonn A. Gaffney. "A method for the inference of cytokine interaction networks". PLOS Computational Biology 18, nr 6 (22.06.2022): e1010112. http://dx.doi.org/10.1371/journal.pcbi.1010112.
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Cell-cell communication is mediated by many soluble mediators, including over 40 cytokines. Cytokines, e.g. TNF, IL1β, IL5, IL6, IL12 and IL23, represent important therapeutic targets in immune-mediated inflammatory diseases (IMIDs), such as inflammatory bowel disease (IBD), psoriasis, asthma, rheumatoid and juvenile arthritis. The identification of cytokines that are causative drivers of, and not just associated with, inflammation is fundamental for selecting therapeutic targets that should be studied in clinical trials. As in vitro models of cytokine interactions provide a simplified framework to study complex in vivo interactions, and can easily be perturbed experimentally, they are key for identifying such targets. We present a method to extract a minimal, weighted cytokine interaction network, given in vitro data on the effects of the blockage of single cytokine receptors on the secretion rate of other cytokines. Existing biological network inference methods typically consider the correlation structure of the underlying dataset, but this can make them poorly suited for highly connected, non-linear cytokine interaction data. Our method uses ordinary differential equation systems to represent cytokine interactions, and efficiently computes the configuration with the lowest Akaike information criterion value for all possible network configurations. It enables us to study indirect cytokine interactions and quantify inhibition effects. The extracted network can also be used to predict the combined effects of inhibiting various cytokines simultaneously. The model equations can easily be adjusted to incorporate more complicated dynamics and accommodate temporal data. We validate our method using synthetic datasets and apply our method to an experimental dataset on the regulation of IL23, a cytokine with therapeutic relevance in psoriasis and IBD. We validate several model predictions against experimental data that were not used for model fitting. In summary, we present a novel method specifically designed to efficiently infer cytokine interaction networks from cytokine perturbation data in the context of IMIDs.
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Chesnokova, Vera, i Shlomo Melmed. "Minireview: Neuro-Immuno-Endocrine Modulation of the Hypothalamic-Pituitary-Adrenal (HPA) Axis by gp130 Signaling Molecules". Endocrinology 143, nr 5 (1.05.2002): 1571–74. http://dx.doi.org/10.1210/endo.143.5.8861.
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Abstract The neuroendocrine and immune systems communicate bidirectionally. The neuro-immune-endocrine interface is mediated by cytokines acting as auto/paracrine or endocrine factors regulating pituitary development, cell proliferation, hormone secretion, and feedback control of the hypothalamic-pituitary-adrenal (HPA) axis. At birth or during neonatal ontogenesis, cytokines produce permanent alterations of HPA axis function and the stress response. Overexpressing IL-6 or leukemia inhibitory factor leads to significant changes in pituitary development and functions. Pituitary corticotroph POMC gene expression is regulated by CRH as well as several gp130 cytokines acting as neuro-immuno-endocrine modulators. Conversely, HPA axis functions modulate susceptibility or resistance to inflammatory disease. Cytokines (including IL-1, TNF, and members of the gp130 cytokine family) participate as mediators of a complex HPA axis response to stress and inflammation. Prolonged exposure to proinflammatory cytokines increases levels of the dominant negative glucocorticoid receptor isoform. Nonresponsiveness of the HPA axis to glucocorticoid negative feedback control provides a defense from destructive effects of cytokine excess. At the same time, gp130 cytokines stimulate pituitary suppressor of cytokine signaling (SOCS)-3, which represses cytokine signaling and abrogates cytokine-induced corticotroph POMC gene transcription and ACTH secretion.
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Kristensen, Nanna Ny, Andreas Nygaard Madsen, Allan Randrup Thomsen i Jan Pravsgaard Christensen. "Cytokine production by virus-specific CD8+ T cells varies with activation state and localization, but not with TCR avidity". Journal of General Virology 85, nr 6 (1.06.2004): 1703–12. http://dx.doi.org/10.1099/vir.0.79903-0.
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The ability of virus-specific CD8+ T cells to produce cytokines was studied in mice infected with lymphocytic choriomeningitis virus and vesicular stomatitis virus. Intracellular staining was used to visualize cytokine-producing CD8+ and CD4+ T cells. Overall, virus-specific CD8+ T cells produce a similar range of cytokines (IFN-γ, TNF-α, IL-2, GM-CSF, RANTES, MIP-1α and MIP-1β) as CD4+ T cells, but the relative distribution of cytokine-producing subsets is different. Moreover, cytokine-producing CD8+ T cells were found to dominate numerically at all time-points tested. Co-staining for more than one cytokine revealed that while all cytokine-producing CD8+ T cells synthesized IFN-γ, additional cytokines were produced by partly overlapping subsets of this population. The frequency of cells producing more than one cytokine was higher in a tertiary site (peritoneum) and generally increased with transition into the memory phase; however, GM-CSF producing cells were only present transiently. Concerning factors predicted to influence the distribution of cytokine-producing subsets, IFN-γ and IL-12 did not play a role, nor was extensive virus replication essential. Notably, regarding the heterogeneity in cytokine production by individual cells with similar epitope specificity, variation in TCR avidity was not the cause, since in vivo-activated TCR transgene-expressing cells were as heterogeneous in cytokine expression as polyclonal cells specific for the same epitope.
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Pawlowski, Kristen D., Joseph T. Duffy, Stephen Gottschalk i Irina V. Balyasnikova. "Cytokine Modification of Adoptive Chimeric Antigen Receptor Immunotherapy for Glioblastoma". Cancers 15, nr 24 (15.12.2023): 5852. http://dx.doi.org/10.3390/cancers15245852.
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Chimeric antigen receptor (CAR) cell-based therapies have demonstrated limited success in solid tumors, including glioblastoma (GBM). GBMs exhibit high heterogeneity and create an immunosuppressive tumor microenvironment (TME). In addition, other challenges exist for CAR therapy, including trafficking and infiltration into the tumor site, proliferation, persistence of CARs once in the tumor, and reduced functionality, such as suboptimal cytokine production. Cytokine modification is of interest, as one can enhance therapy efficacy and minimize off-target toxicity by directly combining CAR therapy with cytokines, antibodies, or oncolytic viruses that alter cytokine response pathways. Alternatively, one can genetically modify CAR T-cells or CAR NK-cells to secrete cytokines or express cytokines or cytokine receptors. Finally, CARs can be genetically altered to augment or suppress intracellular cytokine signaling pathways for a more direct approach. Codelivery of cytokines with CARs is the most straightforward method, but it has associated toxicity. Alternatively, combining CAR therapy with antibodies (e.g., anti-IL-6, anti-PD1, and anti-VEGF) or oncolytic viruses has enhanced CAR cell infiltration into GBM tumors and provided proinflammatory signals to the TME. CAR T- or NK-cells secreting cytokines (e.g., IL-12, IL-15, and IL-18) have shown improved efficacy within multiple GBM subtypes. Likewise, expressing cytokine-modulating receptors in CAR cells that promote or inhibit cytokine signaling has enhanced their activity. Finally, gene editing approaches are actively being pursued to directly influence immune signaling pathways in CAR cells. In this review, we summarize these cytokine modification methods and highlight any existing gaps in the hope of catalyzing an improved generation of CAR-based therapies for glioblastoma.
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Kartashova, O. L., T. M. Pashkova, O. A. Pashinina i N. V. Morozova. "Anticytokine activity and the ability to produce cytokine-like substances of staphylococci isolated from the prostatic secretions in men with symptoms of urogenital infection". Russian Journal of Immunology 24, nr 2 (15.04.2021): 257–60. http://dx.doi.org/10.46235/1028-7221-995-aaa.
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To be causal agents for infectious and inflammatory diseases, the microorganisms should have a pathogenic potential, the framework of which is based on persistence factors that ensure their protection from various effectors of the host's immunity. There is evidence that some microorganisms can have anti-cytokine activity (ACA), and at the same time, many microorganisms many synthesize cytokine-like substances, thus, in fact, exhibit cytokine activity. The aim of the present study was to establish the presence of cytokine-like substances and anti-cytokine activity in Staphylococcus strains isolated from prostate secretions in men with symptoms of urogenital infection. This study involved 24 clinical isolates of different Staphylococci types isolated from the prostate gland secretions in men with symptoms of urogenital infection. Ability of staphylococci to cause changes in the IL-4, IL-6, IL-8, IL-10 and TNFα contents was carried out by co-incubating bacteria suspended in normal saline solution together with cytokine solutions, at a ratio of 1:1 (experimental samples). As a control, a solution of cytokines supplemented by normal saline was used. Concentration of cytokines in experimental and control samples was determined by enzyme immunoassay. Anti-cytokine activity (ACA) was expressed as a percentage (%) of cytokine inactivation in experimental mixtures compared to the controls, cytokine activity, as % of cytokine production in the experimental samples compared to the control.The studied staphylococci showed anti-cytokine activity against IL-4 and IL-10, and exhibited ability to produce IL-6 and TNF. At the same time, among staphylococci, there were strains both showing anti-cytokine activity against IL-8, and producing this cytokine.Among different staphylococcal species isolated from prostate secretions in men with symptoms of urogenital infection, the presence of anti-cytokine activity and the ability to produce cytokines was detected; their production (presence and level) was characterized by intraspecific variability. S. xylosus proved to be the most active cytokine producer, which also have the highest anti-cytokine activity against IL-4.
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Gu, Yinuo, Xu Zuo, Siyu Zhang, Zhuoer Ouyang, Shengyu Jiang, Fang Wang i Guoqiang Wang. "The Mechanism behind Influenza Virus Cytokine Storm". Viruses 13, nr 7 (14.07.2021): 1362. http://dx.doi.org/10.3390/v13071362.
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Influenza viruses are still a serious threat to human health. Cytokines are essential for cell-to-cell communication and viral clearance in the immune system, but excessive cytokines can cause serious immune pathology. Deaths caused by severe influenza are usually related to cytokine storms. The recent literature has described the mechanism behind the cytokine–storm network and how it can exacerbate host pathological damage. Biological factors such as sex, age, and obesity may cause biological differences between different individuals, which affects cytokine storms induced by the influenza virus. In this review, we summarize the mechanism behind influenza virus cytokine storms and the differences in cytokine storms of different ages and sexes, and in obesity.
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Zhou, Rui, Wangjun Bu, Yudan Fan, Ziwei Du, Jian Zhang, Shu Zhang, Jin Sun, Zongfang Li i Jun Li. "Dynamic Changes in Serum Cytokine Profile in Rats with Severe Acute Pancreatitis". Medicina 59, nr 2 (9.02.2023): 321. http://dx.doi.org/10.3390/medicina59020321.
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Background and Objectives: Most published research has only investigated a single timepoint after the onset of severe acute pancreatitis (SAP), meaning that they have been unable to observe the relationship between the dynamic changes in cytokines and SAP progression. In this study, we attempted to reveal the relationship between dynamic changes in cytokine expression levels and SAP disease progression and the relationship between cytokines, using continuous large-scale cytokine detection. Materials and Methods: Seventy rats were randomly assigned to control (Con), sham operation (SO) and SAP groups. The SAP group was randomly allocated to five subgroups at 3, 6, 9, 12 and 15 h after the operation. In the SAP group, 5% sodium taurocholate was injected retrograde into the pancreatic bile duct. Animals in the SO group received a similar incision, a turning over of the pancreas. Control animals did not receive any treatment. We observed the survival, ascites fluid amount, pancreatic histopathological scores and serum amylase activity of SAP rats. We used the cytokine microarray to simultaneously detect 90 cytokines and the dynamic changes in one experiment and to analyze the correlation between cytokine expression and disease progression. Results: The mortality of SAP rats increased with an increase in time. Serum amylase activity, pancreatic histopathological scores and ascites fluid amount were time-dependent. Compared with normal rats, 69 cytokines in SAP rats were significantly changed for at least one timepoint, and 49 cytokines were significantly changed at different timepoints after SAP induction. The changes in inflammatory cytokines were significantly upregulated at 6 and 9 h and 12 h and then significantly decreased. Conclusions: The trend of cytokine expression in SAP rats was not consistent with the disease progression. The cytokine–cytokine receptor interaction and MAPK signal’s dominant cytokines were always highly expressed at various time points over the course of SAP.
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Link, Hans. "The cytokine storm in multiple sclerosis". Multiple Sclerosis Journal 4, nr 1 (luty 1998): 12–15. http://dx.doi.org/10.1177/135245859800400104.
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MS is associated with a cytokine storm characterized by the parallel upregulation of proinflammatory (IFN-g, TNF-a, and b, and IL-12) and immune response-down-regulating (TGF-b, IL-10) cytokines. Also IL-6 and the cytolytic molecule perforin are upregulated. Even when evaluated in individual MS patients over the disease course, no Th1/Th2 dichotomy is obvious but, instead, upregulation of Th1+Th2+Th3 cytokines simultaneously, probably reflecting the complex pathology of MS in lesion size, time and distribution in the indiviual patient. Few correlations have been observed between cytokines and clinical MS variables, though upregulation of TGF-b seems to correlate with benign course and minor disability. Both pro- and antiinflammatory cytokines are also produced by microglia and astrocytes, constituting a CNS-cytokine network that interacts with the cytokine network of the immune system. This complexity is to be kept in mind when searching for cytokine abnormalities in MS.
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Kim, Yong-Ku, i Michael Maes. "The role of the cytokine network in psychological stress". Acta Neuropsychiatrica 15, nr 3 (czerwiec 2003): 148–55. http://dx.doi.org/10.1034/j.1601-5215.2003.00026.x.
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Although a considerable amount of evidence has shown that psychological stress alters peripheral and brain cytokines, the physiological significance of cytokine alteration in psychological stress remains to be elucidated. The aims of this review are to analyze the influence of acute and chronic psychological stresses on the cytokine network in animals and in humans, and to explore the pathophysiological implication of the cytokine changes in psychological stress. Acute psychological stress may increase proinflammatory cytokines both in animals and in humans, and increase T-helper-1 cell cytokines in humans. Investigations into the effect of chronic psychological stress on cytokine production in animals gives mixed results. However, in humans, academic exam stress or care-giver's stress appears to induce a shift in the Th1/Th2 cytokine balance toward a Th2 response and increase proinflammatory cytokines. Psychological stress-induced cytokines stimulate the activity of indoleamine 2,3 dioxygenase (IDO) and could induce serotonin depletion-related disorders such as depression in susceptible individuals. Psychological stress-induced production of cytokines may increase the risk for human diseases, such as cardiovascular disease and exacerbation of autoimmune diseases. Proinflammatory cytokines may also play a regulatory role in glucocorticoid resistance and may be involved in wound healing and skin barrier function alterations. Finally, psychological stress-induced production of cytokines may play a role in neurodegenerative changes in the brain.
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Ramani, Thulasi, Carol S. Auletta, Daniel Weinstock, Barbara Mounho-Zamora, Patricia C. Ryan, Theodora W. Salcedo i Gregory Bannish. "Cytokines". International Journal of Toxicology 34, nr 4 (26.05.2015): 355–65. http://dx.doi.org/10.1177/1091581815584918.
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Over the past 30 years, the world of pharmaceutical toxicology has seen an explosion in the area of cytokines. An overview of the many aspects of cytokine safety evaluation currently in progress and evolving strategies for evaluating these important entities was presented at this symposium. Cytokines play a broad role to help the immune system respond to diseases, and drugs which modulate their effect have led to some amazing therapies. Cytokines may be “good” when stimulating the immune system to fight a foreign pathogen or attack tumors. Other “good” cytokine effects include reduction of an immune response, for example interferon β reduction of neuron inflammation in patients with multiple sclerosis. They may be “bad” when their expression causes inflammatory diseases, such as the role of tumor necrosis factor α in rheumatoid arthritis or asthma and Crohn’s disease. Therapeutic modulation of cytokine expression can help the “good” cytokines to generate or quench the immune system and block the “bad” cytokines to prevent damaging inflammatory events. However, care must be exercised, as some antibody therapeutics can cause “ugly” cytokine release which can be deadly. Well-designed toxicology studies should incorporate careful assessment of cytokine modulation that will allow effective therapies to treat unmet needs. This symposium discussed lessons learned in cytokine toxicology using case studies and suggested future directions.
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Mi, Qing-Sheng, Hong-Zhi He, Seo Kook-Heon i Li Zhou. "Cytokines regulate miRNA expression in islet beta cells (129.41)". Journal of Immunology 178, nr 1_Supplement (1.04.2007): S225—S226. http://dx.doi.org/10.4049/jimmunol.178.supp.129.41.
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Abstract Type 1 diabetes (T1D) results from the autoimmune destruction of insulin-secreting beta cells. The immune system utilizes diverse mediators, including the cytokines, to kill pancreatic beta cells. Accumulating evidence suggests that apoptosis is themain form of beta cell death in spontaneousT1D and islet transplantation, and that the cytokines are key contributors in triggering beta cell apoptosis.MicroRNAs (miRNAs) are a recently discovered class of evolutionarily conserved small noncoding RNAs that lead to post-transcriptional repression, which is involved in the regulation of cell proliferation and cell death. To test the role of miRNAs in cytokine-mediated apoptosis, we compared the miRNA expression profile in rat insulinoma cell line INS-1 (834/40) with or without cytokine treatment, and between cytokine-resistant (INS-1res 833/15) and cytokine-sensitive (INS-1 834/40) cells, using miRNA array. We found that miRNAs were differentially regulated in cytokine-treated INS-1 834/40 compared to untreated cells, and between INS-1 834/40 and INS-1res 833/15 before or after cytokine treatments. Some of these changed miRNAs were recently reported to be linked to control cell growth and apoptosis. These results are the first evidence, to our knowledge, that cytokines can regulate miRNA expression, which suggests that these cytokine-regulated miRNAs could be involved in cytokine-mediated beta cell apoptosis. (JDRF, 5-2006-386)
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Cui, Ang, Teddy Huang, Shuqiang Li, Aileen Ma, Jorge Perez, Chris Sander, Derin Keskin, Catherine Wu, Ernest Fraenkel i Nir Hacohen. "Dictionary of immune responses to 86 cytokines in vivoat single-cell resolution". Journal of Immunology 210, nr 1_Supplement (1.05.2023): 243.18. http://dx.doi.org/10.4049/jimmunol.210.supp.243.18.
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Abstract Cytokines mediate cell-cell communication in the immune system and represent important therapeutic targets. A myriad of studies have underscored their central role in immune function, yet we lack a global view of the cellular responses of each immune cell type to each cytokine. To address this gap we created the Immune Dictionary – a compendium of single-cell transcriptomic profiles of over 20 cell types in response to each of 86 cytokines in murine lymph nodes in vivo, representing over 1,500 cytokine-cell type combinations. A cytokine-centric view of the dictionary revealed that most cytokines induced highly cell type-specific responses. For example, the inflammatory cytokine IL-1β induced distinct gene programs in almost every cell type. A cell type-centric view of the dictionary identified multiple cytokine-driven cellular polarization states in each immune cell type, including previously uncharacterized states such as an IL-18-induced polyfunctional NK cell state. Based on the dictionary, we developed companion software, Immune Response Enrichment Analysis (IREA), for assessing cytokine activities and immune cell polarization from gene expression data, and applied it to reveal cytokine networks in tumors following immune checkpoint blockade therapy. Our dictionary generates new hypotheses for cytokine functions, illuminates pleiotropic effects of cytokines, expands our knowledge of activation states of each immune cell type, and provides a framework to deduce the roles of specific cytokines and cell-cell communication networks in any immune response. This work was supported by the NIH Grant RM1HG006193 and an Adelson Medical Research Foundation Grant to N.H. This work was also supported by a Natural Sciences and Engineering Research Council of Canada (NSERC) Doctoral Fellowship, Whitaker Health Sciences Fund Fellowship, and Wellington and Irene Loh Fund Fellowship to A.C., and NCI Research Specialist Award (R50CA251956) to S.L.
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Li, Yuan, Dan Yang, Bo Sun, Xu Zhang, Fangda Li, Zhili Liu i Yuehong Zheng. "Discovery of crucial cytokines associated with abdominal aortic aneurysm formation by protein array analysis". Experimental Biology and Medicine 244, nr 18 (31.10.2019): 1648–57. http://dx.doi.org/10.1177/1535370219885101.
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As a common disease, abdominal aortic aneurysm (AAA) features permanently progressively dilated abdominal aorta. Various cytokines are implicated in AAA pathogenesis. Clarification of involved cytokines combined with functional analysis may provide new insights into AAA pathogenesis. Using a mouse model, this study analyzed the cytokine profiles in AAA. Cytokines were measured in AAA tissues of saline control or angiotensin II-treated ApoE−/− mice using an antibody array of 200 cytokines, cytokine receptors, and related proteins. Statistical analysis revealed that 21 of 200 proteins were differentially expressed in AAA. These differentially expressed proteins were subjected to function and pathway enrichment analysis, which revealed that leukocyte migration and positive regulation of cell adhesion were the most significant biological processes. Specific signaling pathways, including Janus kinase/signal transducers and activators of transcription and cytokine–cytokine receptor interaction, were prominent in Kyoto encyclopedia of genes and genomes pathway enrichment analysis. Importantly, our data identified cytokines which had not previously been illustrated in AAA pathogenic pathways. Bivariate correlation analysis between these cytokines and protease activity showed that granulocyte colony-stimulating factor (G-CSF), macrophage inflammatory protein 1 g, cardiotrophin 1, milk fat globule-EGF factor 8 protein, interleukin 33, and periostin were positively correlated with matrix metalloprotease 1 (MMP-1), MMP-9, cathepsin B, and cathepsin L. G-CSF was positively correlated with cathepsin L. In conclusion, these results demonstrate that cytokine profile is significantly altered in AAA, and that the newly identified crucial cytokines may function potentially in AAA pathogenesis. Impact statement Various cytokines are known contributors to abdominal aortic aneurysm (AAA) pathologic processes, but the mechanisms underlying the pathogenesis remains unclear. We illustrated the altered cytokine profiles in AAA by high throughput antibody array of 200 cytokines, cytokine receptors and related proteins, as well as bioinformatics analysis of differentially expressed proteins in lesion tissues from AAA mice infused with angiotensin II. Functional analyses of differentially expressed cytokines showed clustering on cell migration and adhesion processes. More importantly, crucial cytokines whose association with AAA formation had not been established were identified. Significant correlations were found between these cytokines and protease activity. This study identifies several crucial markers for further researches on the molecular basis of AAA.
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Freeman, Bailey E., Hans-Peter Raué, Ann B. Hill i Mark K. Slifka. "Cytokine-Mediated Activation of NK Cells during Viral Infection". Journal of Virology 89, nr 15 (20.05.2015): 7922–31. http://dx.doi.org/10.1128/jvi.00199-15.
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ABSTRACTNatural killer (NK) cells provide a first line of defense against infection via the production of antiviral cytokines and direct lysis of target cells. Cytokines such as interleukin 12 (IL-12) and IL-18 are critical regulators of NK cell activation, but much remains to be learned about how cytokines interact to regulate NK cell function. Here, we have examined cytokine-mediated activation of NK cells during infection with two natural mouse pathogens, lymphocytic choriomeningitis virus (LCMV) and murine cytomegalovirus (MCMV). Using a systematic screen of 1,849 cytokine pairs, we identified the most potent combinations capable of eliciting gamma interferon (IFN-γ) production in NK cells. We observed that NK cell responses to cytokine stimulation were reduced 8 days after acute LCMV infection but recovered to preinfection levels by 60 days postinfection. In contrast, during MCMV infection, NK cell responses to cytokines remained robust at all time points examined. Ly49H-positive (Ly49H+) NK cells recognizing viral ligand m157 showed preferential proliferation during early MCMV infection. A population of these cells was still detected beyond 60 days postinfection, but these divided cells did not demonstrate enhanced IFN-γ production in response to innate cytokine stimulation. Instead, the maturation state of the NK cells (as determined by CD11b or CD27 surface phenotype) was predictive of responsiveness to cytokines, regardless of Ly49H expression. These results help define cytokine interactions that regulate NK cell activation and highlight variations in NK cell function during two unrelated viral infections.IMPORTANCENatural killer cells play an important role in immunity to many viral infections. From an initial screen of 1,849 cytokine pairs, we identified the most stimulatory cytokine combinations capable of inducing IFN-γ production by NK cells. Ly49H+NK cells, which can be directly activated by MCMV protein m157, preferentially proliferated during MCMV infection but did not show enhanced IFN-γ production following directex vivocytokine stimulation. Instead, mature CD11b+and/or CD27+NK cells responded similarly to innate cytokine stimulation regardless of Ly49H expression. Collectively, our data provide a better foundation for understanding cytokine-mediated NK cell activation during viral infection.
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Plata-Salaman, Carlos R. "Brain cytokines and disease". Acta Neuropsychiatrica 14, nr 6 (grudzień 2002): 262–78. http://dx.doi.org/10.1034/j.1601-5215.2002.140602.x.
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Cytokines (e.g. various interleukins and subfamily members, tumor necrosis factors, interferons, chemokines and growth factors) act in the brain as immunoregulators and neuromodulators. Over a decade ago, the integrative article ‘Immunoregulators in the Nervous System’ (Neurosci Biobehav Rev1991; 15: 185–215) provided a comprehensive framework of pivotal issues on cytokines and the nervous system that recently have been extensively studied. Cytokine profiles in the brain, including cytokine generation and action, have been studied in multiple models associated with neuropathophysiological conditions. These include: (1) acute conditions and disorders such as stroke (cerebral ischemia or infarction and intracranial hemorrhage), traumatic brain injury, spinal cord injury and acute neuropathies; (2) chronic neurodegenerative disorders and chronic conditions, including Alzheimer's disease, Parkinson's disease, neuropathic pain, epilepsy and chronic neuropathies; (3) brain infections, including bacterial meningitis and encephalitis; (4) brain tumors; (5) neuroimmunological disorders per se, such as multiple sclerosis; (5) psychiatric disorders, including schizophrenia and depression; (6) neurological and neuropsychiatric manifestations associated with non- central nervous system (CNS) disorders such as peripheral cancer, liver, kidney and metabolic compromise, and peripheral infectious and inflammatory conditions; and (7) cytokine immunotherapy, which can be accompanied by neuropsychiatric manifestations when administered either via peripheral or brain routes. Cytokine profiles have also been studied in multiple animal models challenged with inflammatory, infectious, chemical, malignant and stressor insults. Essentially data show that cytokines play a pivotal role in multiple neuropathophysiological processes associated with different types of disorders and insults. Cytokine expression and action in the brain shows a different profile across conditions, but some similarities exist. Under a defined temporal sequence, cytokine involvement in neuroprotection or the induction of a deleterious pathophysiological cascade and in resolution/healing is proposed depending on the type of cytokine. In the brain, functional interactions among cytokines, balance between pro-inflammatory and anti-inflammatory cytokines and functional interactions with neurotransmitters and neuropeptides play a pivotal role in the overall cytokine profile, pattern of neuropathophysiological cascades, and quality and magnitude of neuropsychiatric manifestations. In this brief review various selected cytokine-related issues with relevance to the brain are discussed.
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Patil, Agraja, i Swapna Mahale. "Cytokines and anti-cytokine therapy in periodontal disease". IOSR Journal of Dental and Medical Sciences 16, nr 03 (kwiecień 2017): 63–70. http://dx.doi.org/10.9790/0853-1603026370.
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Whiteside, T. L. "Cytokines and cytokine measurements in a clinical laboratory." Clinical and diagnostic laboratory immunology 1, nr 3 (1994): 257–60. http://dx.doi.org/10.1128/cdli.1.3.257-260.1994.
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Deswal, Anita, Nancy J. Petersen, Arthur M. Feldman, James B. Young, Bill G. White i Douglas L. Mann. "Cytokines and Cytokine Receptors in Advanced Heart Failure". Circulation 103, nr 16 (24.04.2001): 2055–59. http://dx.doi.org/10.1161/01.cir.103.16.2055.
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