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1
Trinchieri, Giorgio. "Cytokines and cytokine receptors." Immunological Reviews 202, no. 1 (December 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, no. 1 (1992): 33–34. http://dx.doi.org/10.1007/bf00331973.
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Berti, E., and R. Caputo. "Cytokines, cytokine receptors and cytokine antibodies." Melanoma Research 6, SUPPLEMENT 1 (September 1996): S25. http://dx.doi.org/10.1097/00008390-199609001-00064.
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van Deventer, S. J. H. "Cytokines and cytokine-based therapies." Current Opinion in Gastroenterology 14, no. 4 (July 1998): 317–21. http://dx.doi.org/10.1097/00001574-199807000-00008.
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Li, Aileen W., and Wendell A. Lim. "Engineering cytokines and cytokine circuits." Science 370, no. 6520 (November 26, 2020): 1034–35. http://dx.doi.org/10.1126/science.abb5607.
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Burger, D., and J. M. Dayer. "Inhibitory cytokines and cytokine inhibitors." Neurology 45, Issue 6, Supplement 6 (June 1, 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, and Stephen Hefeneider. "Cytokine Modulation of Keratinocyte Cytokines." Journal of Investigative Dermatology 94, no. 6 (June 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, no. 9-10 (October 2006): 1089–105. http://dx.doi.org/10.1016/j.addr.2006.07.014.
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Ramani, Thulasi, Carol S. Auletta, Daniel Weinstock, Barbara Mounho-Zamora, Patricia C. Ryan, Theodora W. Salcedo, and Gregory Bannish. "Cytokines." International Journal of Toxicology 34, no. 4 (May 26, 2015): 355–65. http://dx.doi.org/10.1177/1091581815584918.
Повний текст джерелаАнотація:
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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Standiford, Theodore. "Anti-inflammatory Cytokines and Cytokine Antagonists." Current Pharmaceutical Design 6, no. 6 (April 1, 2000): 633–49. http://dx.doi.org/10.2174/1381612003400533.
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BARRY, M., and G. McFADDEN. "Virus encoded cytokines and cytokine receptors." Parasitology 115, no. 7 (December 1997): 89–100. http://dx.doi.org/10.1017/s0031182097001820.
Повний текст джерелаАнотація:
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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Olbei, M., D. Modos, D. Cozzetto, N. Powell, and 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 (January 30, 2023): i236. http://dx.doi.org/10.1093/ecco-jcc/jjac190.0200.
Повний текст джерелаАнотація:
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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Łabędź, Wojciech, Anna Przybyla, Agnieszka Zimna, Mikołaj Dąbrowski, and Łukasz Kubaszewski. "The Role of Cytokines in the Metastasis of Solid Tumors to the Spine: Systematic Review." International Journal of Molecular Sciences 24, no. 4 (February 14, 2023): 3785. http://dx.doi.org/10.3390/ijms24043785.
Повний текст джерелаАнотація:
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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Lin, Jian-Xin, and Warren J. Leonard. "Fine-Tuning Cytokine Signals." Annual Review of Immunology 37, no. 1 (April 26, 2019): 295–324. http://dx.doi.org/10.1146/annurev-immunol-042718-041447.
Повний текст джерелаАнотація:
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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Buxton, Miatta A., Noemi Meraz-Cruz, Brisa N. Sánchez, Betsy Foxman, Carina J. Gronlund, Jorge Beltran-Montoya, Marisol Castillo-Castrejon, Marie S. O'Neill, and Felipe Vadillo-Ortega. "Repeated Measures of Cervicovaginal Cytokines during Healthy Pregnancy: Understanding “Normal” Inflammation to Inform Future Screening." American Journal of Perinatology 37, no. 06 (April 12, 2019): 613–20. http://dx.doi.org/10.1055/s-0039-1685491.
Повний текст джерелаАнотація:
Abstract Objective This study aimed to describe characteristics of cervicovaginal cytokines obtained during pregnancy from women who subsequently delivered at term. Study Design We used repeated measures of 20 cervicovaginal cytokines, collected on average on a monthly basis, from the second to the ninth month of gestation among 181 term pregnancies in the Mexico City Pregnancy Research on Inflammation, Nutrition, & City Environment: Systematic Analyses cohort (2009–2014). Cytokines were quantified using multiplex assay. Results Cytokine distributions differed more between than within cytokines. Across trimesters, cytokines interleukin (IL)-1Ra, IL-1α, and IL-8 consistently had high concentrations compared with other measured cytokines. Cytokine intraclass correlation coefficients ranged from 0.41 to 0.82. Spearman's correlation coefficients among cytokine pairs varied but correlation directions were stable; 95.3% of the 190 correlation pairs remained either negative or positive across trimesters. Mean longitudinal patterns of log-transformed cytokines from Tobit regression varied across but less within cytokines. Conclusion Although mean concentrations of cervicovaginal cytokines among term pregnancies were high, they were largely stable over time. The high cytokine concentrations corroborate that pregnancy is associated with an active inflammatory state. These characterizations may serve as a baseline for comparison to other obstetric outcomes, which may be helpful in understanding deviations from normal gestational inflammation.
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Hong, Chang-Sook, Brenda Diergaarde, and 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, no. 18_Supplement (September 15, 2023): PO—096—PO—096. http://dx.doi.org/10.1158/1557-3265.aacrahns23-po-096.
Повний текст джерелаАнотація:
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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Yuwen, Li, Yang Ciqiu, Shi Yi, Liu Ruilei, Lai Yuanhui, Lin Bo, Li Songqi, Lv Weiming, and Li Jie. "A Pilot Study of Protein Microarray for Simultaneous Analysis of 274 Cytokines Between Abdominal Aortic Aneurysm and Normal Aorta." Angiology 70, no. 9 (April 24, 2019): 830–37. http://dx.doi.org/10.1177/0003319719844678.
Повний текст джерелаАнотація:
Cytokines play an important role in the pathogenesis of abdominal aortic aneurysm (AAA). We evaluated the cytokine expression profile of large AAA walls using a 274-cytokine protein array. We hypothesized that AAAs are characterized by an inflammatory, chemotactic cytokine profile. We investigated the cytokine expression profile of 12 patients with AAA and 6 nonaneurysmal controls using an antibody-based protein array. The array generated antibodies against homogenized human aortic tissues to validate the cytokines differentially expressed in AAAs and normal aortas. Data were quantified using fluorescent signal intensities and statistically analyzed by the t test. Fifty-nine cytokines were differentially expressed between the AAA and control samples. Of the 35 selected cytokines that had relative expression >1000, 29 were significantly higher and 6 were lower in AAA samples than in controls. They respectively belonged to CC chemokines, CXC chemokines, pro-inflammatory cytokines, growth factors, proteolytic proteins and inhibitors, and cell adhesion cytokines. Our results show that distinct cytokines are involved in AAAs and suggest that the pathways involving these cytokines may be associated with the pathogenesis and development of AAAs. These findings, if confirmed by larger studies, may suggest treatment targets.
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Debets, R., and H. F. J. Savelkoul. "Cytokines as cellular communicators." Mediators of Inflammation 5, no. 6 (1996): 417–23. http://dx.doi.org/10.1155/s0962935196000579.
Повний текст джерелаАнотація:
Cytokines and their receptors are involved in the pathophysiology of many diseases. Here we present a detailed review on cytokines, receptors and signalling routes, and show that one important lesson from cytokine biology is the complex and diverse regulation of cytokine activity. The activity of cytokines is controlled at the level of transcription, translation, storage, processing, posttranslational modification, trapping, binding by soluble proteins, and receptor number and/or function. Translation of this diverse regulation in strategies aimed at the control of cytokine activity will result in the development of more specific and selective drugs to treat diseases.
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Cai, Rui. "Progress in the application of cytokines in lung cancer treatment." Highlights in Science, Engineering and Technology 74 (December 29, 2023): 378–85. http://dx.doi.org/10.54097/zq3ga069.
Повний текст джерелаАнотація:
Lung cancer is the most common cancer today and has become the leading cause of cancer death worldwide. Previous common therapy of this disease mainly include surgery, radiation therapy, chemotherapy etc., and the recently most focused solution of immunotherapy, therapy making use of immunity agents such as vaccines, monoclonal antibodies and cytokines. Cytokines, such as gefitinib, the epidermal growth factor receptor inhibitor, and bevacizumab, the VEGF inhibitor, have been widely used in the clinic as targets for the treatment of lung cancer. Another application of cytokines in the treatment of lung cancer is to play the role of biomarkers to provide an important judgment basis for prognosis and diagnosis. However, based on understanding of the advantages and limitations of cytokine therapy, scientists have ceased to make efforts to develop it into a core of the cancer therapy. cytokine’s potential to be combined with other therapies and to play indicative roles in cancer treatment still arouses scientists’ interest. This passage reviews the common treatments of lung cancer and discusses the progress in the application of cytokines as a component of cancer treatment.
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Li, Yuan, Dan Yang, Bo Sun, Xu Zhang, Fangda Li, Zhili Liu, and Yuehong Zheng. "Discovery of crucial cytokines associated with abdominal aortic aneurysm formation by protein array analysis." Experimental Biology and Medicine 244, no. 18 (October 31, 2019): 1648–57. http://dx.doi.org/10.1177/1535370219885101.
Повний текст джерелаАнотація:
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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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, and S. A. Nedospasov. "Cytokines, reverse genetics and anti-cytokine therapy." Bulletin of Siberian Medicine 18, no. 1 (May 16, 2019): 38–48. http://dx.doi.org/10.20538/1682-0363-2019-1-38-48.
Повний текст джерелаАнотація:
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., and Warren J. Leonard. "Cytokine signaling: Inhibitors keep cytokines in check." Current Biology 9, no. 23 (December 1999): R899—R902. http://dx.doi.org/10.1016/s0960-9822(00)80079-2.
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Cui, Ang, Teddy Huang, Shuqiang Li, Aileen Ma, Jorge Perez, Derin Keskin, Chris Sander, Catherine J. Wu, Ernest Fraenkel, and Nir Hacohen. "Systematic dissection of cytokine responses in vivo at single-cell resolution." Journal of Immunology 206, no. 1_Supplement (May 1, 2021): 106.13. http://dx.doi.org/10.4049/jimmunol.206.supp.106.13.
Повний текст джерелаАнотація:
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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Kim, Yong-Ku, and Michael Maes. "The role of the cytokine network in psychological stress." Acta Neuropsychiatrica 15, no. 3 (June 2003): 148–55. http://dx.doi.org/10.1034/j.1601-5215.2003.00026.x.
Повний текст джерелаАнотація:
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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Lin, Sheng-Chieh, Li-Shian Shi, and Yi-Ling Ye. "Advanced Molecular Knowledge of Therapeutic Drugs and Natural Products Focusing on Inflammatory Cytokines in Asthma." Cells 8, no. 7 (July 5, 2019): 685. http://dx.doi.org/10.3390/cells8070685.
Повний текст джерелаАнотація:
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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Plata-Salaman, Carlos R. "Brain cytokines and disease." Acta Neuropsychiatrica 14, no. 6 (December 2002): 262–78. http://dx.doi.org/10.1034/j.1601-5215.2002.140602.x.
Повний текст джерелаАнотація:
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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Plata-Salamán, Carlos R. "Cytokines and Feeding." Physiology 13, no. 6 (December 1998): 298–304. http://dx.doi.org/10.1152/physiologyonline.1998.13.6.298.
Повний текст джерелаАнотація:
Cytokines inhibit feeding through peripheral and brain mechanisms. Behavioral, cellular, and molecular studies show that interactions among cytokines, neurotransmitters, and peptides and modulation of hypothalamic neurons are involved in cytokine-induced feeding inhibition. This action of cytokines is relevant to the control of feeding in health and disease.
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Chesnokova, Vera, and Shlomo Melmed. "Minireview: Neuro-Immuno-Endocrine Modulation of the Hypothalamic-Pituitary-Adrenal (HPA) Axis by gp130 Signaling Molecules." Endocrinology 143, no. 5 (May 1, 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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Cannon, J. G., J. L. Nerad, D. D. Poutsiaka, and C. A. Dinarello. "Measuring circulating cytokines." Journal of Applied Physiology 75, no. 4 (October 1, 1993): 1897–902. http://dx.doi.org/10.1152/jappl.1993.75.4.1897.
Повний текст джерелаАнотація:
Cytokines, i.e., regulatory proteins derived primarily (but not exclusively) from cells of the immune system, are receiving increasing attention for their influences on physiological processes. This paper outlines several of the unique characteristics of cytokines and discusses the pitfalls encountered when measuring them in biological fluids. At present, each available assay has a combination of advantages and drawbacks; therefore, investigators must be aware of the trade-offs and choose the assay that best addresses their needs. The factors that affect cytokine measurement also influence cytokine activity in vivo; thus they are important from a physiological as well as methodological standpoint. Moreover, the absolute concentration of a single cytokine is probably less important than the balance between that cytokine and its natural antagonists.
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Feliciani, C., A. K. Gupta, and D. N. Saucier. "Keratinocytes and Cytokine/Growth Factors." Critical Reviews in Oral Biology & Medicine 7, no. 4 (October 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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Borge, Bengt Åge Sørby, Karl-Henning Kalland, Sue Olsen, Athanasia Bletsa, Ellen Berggreen, and Helge Wiig. "Cytokines are produced locally by myocytes in rat skeletal muscle during endotoxemia." American Journal of Physiology-Heart and Circulatory Physiology 296, no. 3 (March 2009): H735—H744. http://dx.doi.org/10.1152/ajpheart.01309.2008.
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Cytokines act as chemical mediators during the inflammatory process. Measurements of cytokine levels in tissue have previously been performed in homogenized tissue, but the true concentrations in native interstitial fluid (ISF), i.e., the compartment where cytokines exert their biologically active role, have remained unknown. The role of skeletal muscle myocytes as a source for cytokines during endotoxemia was explored by collecting muscle ISF using a wick method, and the levels of 14 cytokines in ISF and plasma were related to the corresponding changes in mRNA levels to reveal any potential discrepancies between gene expression and protein release of cytokines to ISF. The majority of investigated cytokines were elevated in muscle ISF during endotoxemia, and an analysis of cytokine mRNA levels revealed consistency between gene expression and protein release. The elevated cytokine level in ISF, in addition to elevated gene expression in muscle, indicated a significant local production and release of several proinflammatory cytokines and chemokines within skeletal muscle tissue during endotoxemia. Immunohistochemistry revealed that myocytes constituted a significant source of IL-1β and TNF-α production during endotoxemia, whereas the contribution from inflammatory cells i.e., leukocytes, was found to be less significant. Muscle cells apparently constitute an important source of several different cytokines during endotoxemia, governing the level in the muscle microenvironment, and are likely to contribute significantly to cytokine levels in plasma.
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Lucey, D. R., M. Clerici, and G. M. Shearer. "Type 1 and type 2 cytokine dysregulation in human infectious, neoplastic, and inflammatory diseases." Clinical Microbiology Reviews 9, no. 4 (October 1996): 532–62. http://dx.doi.org/10.1128/cmr.9.4.532.
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In the mid-1980s, Mosmann, Coffman, and their colleagues discovered that murine CD4+ helper T-cell clones could be distinguished by the cytokines they synthesized. The isolation of human Th1 and Th2 clones by Romagnani and coworkers in the early 1990s has led to a large number of reports on the effects of Th1 and Th2 on the human immune system. More recently, cells other than CD4+ T cells, including CD8+ T cells, monocytes, NK cells, B cells, eosinophils, mast cells, basophils, and other cells, have been shown to be capable of producing "Th1" and "Th2" cytokines. In this review, we examine the literature on human diseases, using the nomenclature of type 1 (Th1-like) and type 2 (Th2-like) cytokines, which includes all cell types producing these cytokines rather than only CD4+ T cells. Type 1 cytokines include interleukin-2 (IL-2), gamma interferon, IL-12 and tumor necrosis factor beta, while type 2 cytokines include IL-4, IL-5, IL-6, IL-10, and IL-13. In general, type 1 cytokines favor the development of a strong cellular immune response whereas type 2 cytokines favor a strong humoral immune response. Some of these type 1 and type 2 cytokines are cross-regulatory. For example, gamma interferon and IL-12 decrease the levels of type 2 cytokines whereas IL-4 and IL-10 decrease the levels of type 1 cytokines. We use this cytokine perspective to examine human diseases including infections due to viruses, bacteria, parasites, and fungi, as well as selected neoplastic, atopic, rheumatologic, autoimmune, and idiopathic-inflammatory conditions. Clinically, type 1 cytokine-predominant responses should be suspected in any delayed-type hypersensitivity-like granulomatous reactions and in infections with intracellular pathogens, whereas conditions involving hypergammaglobulinemia, increased immunoglobulin E levels, and/or eosinophilia are suggestive of type 2 cytokine-predominant conditions. If this immunologic concept is relevant to human diseases, the potential exists for novel cytokine-based therapies and novel cytokine-directed preventive vaccines for such diseases.
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Alvarez-Rodríguez, L., M. Lopez-Hoyos, C. Mata, M. Jose Marin, J. Calvo-Alen, R. Blanco, E. Aurrecoechea, M. Ruiz-Soto, and V. M. Martínez-Taboada. "Circulating cytokines in active polymyalgia rheumatica." Annals of the Rheumatic Diseases 69, no. 01 (March 1, 2009): 263–69. http://dx.doi.org/10.1136/ard.2008.103663.
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Objective:To characterise the circulating cytokine profile and the cellular source of circulating cytokines in polymyalgia rheumatica (PMR).Methods:The study included 34 patients with active untreated PMR and 17 age-matched healthy controls (HC). Circulating cytokines were measured by cytometric bead array and ELISA. Intracellular cytokines were assessed in CD3+ and CD14+ cells by flow cytometry. Cytokines in cell culture supernatants were also determined after polyclonal stimulation of patients’ peripheral blood mononuclear cells.Results:Circulating levels of interleukin-6 (IL6) were significantly higher in subjects with active PMR than in HC. Corticosteroid (CS) treatment was followed by a decrease in the level of IL6. Intracellular cytokine staining showed that circulating monocytes did not produce higher amounts of proinflammatory cytokines in patients with PMR than in HC. There was a discordance between serum levels and cytokine-producing monocyte and T cells, and it was not possible to demonstrate a Th1 bias in the peripheral compartment.Conclusions:Active PMR is characterised by increased serum levels of IL6, but not of other proinflammatory cytokines, that are rapidly suppressed by CS treatment. As circulating monocytes do not show increased production of proinflammatory cytokines, IL6 may be mainly produced in the inflamed tissue. A study of the circulating cytokine profile and its cellular source may provide a clue to new therapeutic options.
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Maecker, Holden T., Weiqi Wang, Yael Rosenberg-Hasson, Richard C. Semelka, Joseph Hickey, and Lorrin M. Koran. "An initial investigation of serum cytokine levels in patients with gadolinium retention." Radiologia Brasileira 53, no. 5 (October 2020): 306–13. http://dx.doi.org/10.1590/0100-3984.2019.0075.
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Abstract Objective: To determine whether individuals with proposed gadolinium deposition disease (GDD) have elevated serum levels of pro-inflammatory and pro-fibrotic cytokines, and whether specific cytokines are correlated with certain symptoms. Materials and Methods: Twenty-four participants recruited between May 2016 and June 2017 met GDD diagnostic criteria. The 64 control subjects provided serum samples before prophylactic flu vaccination. Serum cytokine levels were obtained with Luminex serum cytokine assay using eBiosciences/Affymetrix human 62-plex kits. Wilcoxon rank-sum tests were performed to assess the difference between the median fluorescence intensity values for the participants and the control group. Generalized linear models were built to evaluate the association between each cytokine of interest and selected participant symptoms. Results: Serum levels of 14 cytokines, including nine pro-inflammatory cytokines, were statistically significantly elevated compared to controls (p ≤ 0.05). Hypotheses regarding pro-fibrotic cytokines and cytokine links to specific symptoms’ intensity were not confirmed. Conclusion: The statistically significantly elevated cytokines may be markers of susceptibility to GDD or agents of symptom induction. These findings suggest that individuals developing symptoms characteristic of GDD after a contrast-assisted magnetic resonance imaging should be studied to investigate whether gadolinium retention and elevated cytokines may be related to their symptoms.
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Olbei, M., J. Thomas, I. Hautefort, A. Treveil, B. Bohar, M. Madgwick, L. Gul, L. Csabai, D. Modos, and 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 (January 1, 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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Simbirtsev, A. S. "Immunopharmacological aspects of the cytokine system." Bulletin of Siberian Medicine 18, no. 1 (May 16, 2019): 84–95. http://dx.doi.org/10.20538/1682-0363-2019-1-84-95.
Повний текст джерелаАнотація:
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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Olson, Matthew Richard, and Mark H. Kaplan. "Autocrine and paracrine cytokine feedback augment the production of Th2-associated cytokines." Journal of Immunology 196, no. 1_Supplement (May 1, 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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Dieleman, L. A., C. O. Elson, G. S. Tennyson, and K. W. Beagley. "Kinetics of cytokine expression during healing of acute colitis in mice." American Journal of Physiology-Gastrointestinal and Liver Physiology 271, no. 1 (July 1, 1996): G130—G136. http://dx.doi.org/10.1152/ajpgi.1996.271.1.g130.
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The mechanisms of wound healing in the gut are poorly understood but are mediated by cytokines in other tissues. In this study we wanted to determine which cytokines were expressed after nonspecific colonic injury, the kinetics of that expression, and how cytokine expression correlated with tissue histology. At 0, 4, 8, 12, 24, 48, and 72 h after intrarectal administration of 3% acetic acid to C3H/HeJ mice, their colons were removed for histology, organ culture, and RNA extraction. Cytokine mRNA expression for various cytokines was assessed by reverse transcriptase-polymerase chain reaction with primers specific for each cytokine. Cytokine production in organ cultures was measured with bioassays. Shortly after colonic injury and during colonic regeneration, proinflammatory cytokines such as interleukin-1 beta (IL-1 beta), IL-6, tumor necrosis factor-alpha (TNF-alpha), macrophage inflammatory protein (MIP), and transforming growth factor-beta (TGF-beta) were expressed. In contrast, expression of T cell-derived cytokines was not detected at any time point. Cytokines such as IL-1 beta, IL-6, IL-10, TNF-alpha, and MIP-1 are important mediators of tissue repair and restitution after nonspecific colonic injury and may subserve a similar role in human colitis.
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Townsend, M. J., and A. N. McKenzie. "Unravelling the net? cytokines and diseases." Journal of Cell Science 113, no. 20 (October 15, 2000): 3549–50. http://dx.doi.org/10.1242/jcs.113.20.3549a.
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The Cytokine Network edited by Fran Balkwill Frontiers in Molecular Biology Series (seried editors B. D. Hames and D. M. Glover) Oxford University Press (2000) pp. 199. ISBN 019–963-702-4. 29.95 Cytokines are small- to medium-sized proteins and glycoproteins that mediate highly potent biological effects on many cell types. They have critical roles in haematopoiesis, inflammatory responses and the development and maintenance of immune responses. Importantly, cytokines act in networks or cascades. Typical properties of cytokines in these networks are pleiotropy, redundancy, synergistic activity and antagonistic effects upon each other. Knowledge of how these networks are comprised and operate is important in understanding how cytokines mediate their diverse effects on biological systems. In The Cytokine Network, Fran Balkwill brings together some distinguished investigators to produce a survey, in eight independently written and concise chapters, of the complex cytokine and chemokine (chemotactic cytokine) networks present in mouse and man. The ever-increasing complexity of cytokine networks is introduced in the initial chapter with a summary of the bioinformatics approach for the high throughput discovery of novel cytokines and chemokines. The burgeoning number of newly identified chemokines, chemokine receptors and TNF family members reminds us that our understanding of the cytokine network is extremely dynamic and that our interpretation of some pathways will change with the characterisation of new factors. The following chapters address the interactions of the cytokines, both with reference to their signalling pathways (well summarised in chapter 2) and their biological roles. The point is made that cytokines should be studied as a network rather than individually and that in vivo models, including the generation of transgenic and gene knock-out mice, are powerful tools for doing so. Rheumatoid arthritis is presented as a well-studied example of how inappropriate regulation of pro- and anti-inflammatory cytokines mediates autoimmune disease, and examples of immunoregulatory cytokines that have both overlapping and independent regulatory effects on inflammation are demonstrated within this context. The important Th1/Th2 paradigm receives a dedicated chapter. T helper type 1 and T helper type 2 cells produce distinct and restricted patterns of cytokines that cross regulate each other and thus mediate different types of immune response. The development of these subsets of T helper cells from a common precursor, as part of a developing immune response, has important effects on the cytokine network. The mechanisms of Th1/Th2 development together with modulating factors and associated intracellular signalling are well described. The chapter summarises well the role of Th1/Th2 development in human diseases with reference to transplantation immunology, neonatal development, autoimmune diseases, and atopic diseases. A very interesting review of the relationships between cytokines and viruses is given. Cytokines are critically involved in mediating antiviral immune responses. However, homologues of cytokines, chemokines and their receptors, after being ‘hijacked’ from the host genome and undergoing evolution along with the viral genes, are utilised by viruses themselves to promote their replication and to suppress immune responses against them. The chapter describes several noteworthy examples of these virally encoded cytokines and receptors together with their roles in vivo. This is a well-written book that provides a good introduction to understanding how cytokines and chemokines interact as a network in the immune system. The volume links together diverse subjects that include cytokine signalling, genomic polymorphism, disease processes and immunotherapies. The book does not aim to describe comprehensively the biology of all the currently known cytokines and chemokines and therefore alternative texts should be considered for this. (ABSTRACT TRUNCATED)
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Zheng, Song, and Wu Wang. "Proinflammatory cytokine and cancer." American Journal of BioMedicine 4, no. 3 (July 11, 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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Nikovics, Krisztina, Anne-Laure Favier, Mathilde Rocher, Céline Mayinga, Johanna Gomez, Frédérique Dufour-Gaume, and Diane Riccobono. "In Situ Identification of Both IL-4 and IL-10 Cytokine–Receptor Interactions during Tissue Regeneration." Cells 12, no. 11 (May 31, 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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Beck, P. L., and J. L. Wallace. "Cytokines in inflammatory bowel disease." Mediators of Inflammation 6, no. 2 (1997): 95–103. http://dx.doi.org/10.1080/09629359791785.
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Over the past decade, much has been learned regarding the role of various cytokines in the pathogenesis of inflammatory bowel disease. Several cytokine ‘knockout’ models in mice have been shown to develop colitis, while alterations in the production of various cytokines has been documented in human Crohn's disease and ulcerative colitis. In recent years, attempts have been made to treat these diseases through modulation of cytokine production or action. This review focuses on the cytokines that have been implicated in the pathogenesis of inflammatory bowel disease. The evidence for and against a role for particular cytokines in intestinal inflammation is reviewed, as is the experimental and clinical data suggesting that cytokines are rational targets for the development of new therapies.
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Dueck, Amylou C., Charles S. Cleeland, Robert Dantzer, Jeff Sloan, Srdan Verstovsek, Robyn M. Emanuel, Holly Lynn Geyer, and Ruben A. Mesa. "Cytokine Profile Changes In 309 Myelofibrosis Patients: Comparison Of JAK1/JAK2 Inhibitor Therapy Vs. Placebo – Correlative Analysis From The Comfort-I Trial." Blood 122, no. 21 (November 15, 2013): 4074. http://dx.doi.org/10.1182/blood.v122.21.4074.4074.
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Abstract Background Inflammatory deregulation may be a major factor in cancer related symptoms (Dantzer Nature Rev Clin Oncol 2012). Improved symptoms in myelofibrosis (MF) patients treated with single arm ruxolitinib (JAK1/JAK2 inhibitor) studies has been correlated with normalization of selected cytokines increased pre-therapy (c-reactive protein, IL-1ra, MIP-1b, TNF-a, and IL-6; Verstovsek NEJM 2010). We sought to assess the impact of JAK1/JAK2 inhibitor therapy on cytokine levels and the relationship between cytokine levels and symptoms prior to and during JAK1/JAK2 inhibitor therapy in the phase III placebo controlled COMFORT-I trial (Verstovsek NEJM 2012). Methods Cytokine levels (89 cytokines measured at baseline and at weeks 4 and 24) and MF symptoms (assessed by MFSAF 2.0 – Mesa JCO 2013) were collected during the blinded phase of COMFORT-I. Patients were randomized to ruxolitinib vs. placebo. Plasma was used for the measurement of cytokines using Rules-Based Medicine, Inc. (Austin, TX) Human MAP panel. Associations between the MFSAF total symptom score (TSS) and log2-transformed cytokine data were investigated at baseline using Spearman correlations and linear regression. Mixed models were used to assess cytokine and TSS changes over time within each arm and overall. Logistic regression was used to assess the relationship between baseline cytokines and TSS response (>/=50% reduction from baseline) at week 24, and between week 4 cytokine changes and TSS response (>/=50% reduction from baseline) at week 24 within each arm and overall. Mixed and logistic regression models combining data across arms also included terms for visit, arm, and visit-by-arm interaction. All models also included age, gender, and body mass index (BMI). Given the large number of cytokines being investigated, p<0.001 was considered statistically significant. Cytokine values below the limit of detection were set at the lowest limit of detection and 25 cytokines were excluded from statistical analysis due to having more than 30% of data missing or below the limit of detection. Results Patients: 309 subjects were randomized in COMFORT-I with median age 68 (range 40-91), 46% female, 50% primary myelofibrosis, and 61% high risk. All 309 subjects had cytokines measured at one or more of the three visits included in this analysis, with 308 having cytokine values paired with a TSS score at the same visit. Cytokines at Baseline: At baseline, the highest Spearman correlations with symptomatic burden (as assessed by the TSS) were observed for APOA1 (rho=-.21) and FERRITIN (rho=-.20), followed by INTLK5, MIP1A, MMP3, INTLK2, MGB, INTLK1A, and INTLK7 with correlations between -.15 and -.17 (all p<0.01). After adjusting for age, sex, and BMI, VCAM1 and APOA1 were significantly associated with TSS at baseline. Cytokine and Symptom changes during trial: Changing levels of 5 cytokines were significantly associated with change of TSS over time beyond the change due to visit, arm, visit-by-arm interaction, age, sex and BMI including VCAM1, LEPTIN, TIMP1, B2MICG, and TNFRII. Within the placebo arm, only 5 cytokines significantly changed over time compared to 46 cytokines in the ruxolitinib arm (visit-by-arm interaction was significant for 43 in the overall models). VCAM1, B2MICG, and TNFRII were among the 5 cytokines which changed in the placebo arm, and VCAM1, LEPTIN, TIMP1, B2MICG, and TNFRII were among the 46 cytokines which changed in the ruxolitinib arm. No baseline cytokines and no changes in cytokines at week 4 univariately predicted week 24 TSS response within either arm at the p<0.001 level. Conclusions In the first serial assessment of MF symptoms and plasma cytokine levels in the conduct of a placebo controlled trial we found 5 cytokines in which improved levels correlated with decreased MF symptom burden in ruxolitinib treated patients. Development of a multivariate model for predicting symptom response, correlations with splenic response and impact on survival benefit of therapy is ongoing. Disclosures: No relevant conflicts of interest to declare.
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Jacob, C. O. "Cytokines and anti-cytokines." Current Opinion in Immunology 2, no. 2 (January 1989): 249–57. http://dx.doi.org/10.1016/0952-7915(89)90196-9.
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Zhou, Rui, Wangjun Bu, Yudan Fan, Ziwei Du, Jian Zhang, Shu Zhang, Jin Sun, Zongfang Li, and Jun Li. "Dynamic Changes in Serum Cytokine Profile in Rats with Severe Acute Pancreatitis." Medicina 59, no. 2 (February 9, 2023): 321. http://dx.doi.org/10.3390/medicina59020321.
Повний текст джерелаАнотація:
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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Corwin, Elizabeth J. "Understanding Cytokines Part I: Physiology and Mechanism of Action." Biological Research For Nursing 2, no. 1 (July 2000): 30–40. http://dx.doi.org/10.1177/109980040000200104.
Повний текст джерелаАнотація:
This is the first of a 2-part article on understanding cytokines. Cytokines are intercellular signaling proteins released from virtually all nucleated cells that influence growth and cellular proliferation in a wide range of tissues. Cytokines have immune modulating effects and are understood to control most of the physical and psychological symptoms associated with infection and inflammation. Cytokines also influence reproduction and bone remodeling. Dysregulation of the cytokine cellular system has significant implications in the development of a variety of illnesses, including most autoimmune disorders, many diseases of the cardiovascular system, osteoporosis, asthma, and depression. For nurses to be adequately informed when caring for clients with chronic illnesses and to be sufficiently knowledgeable when evaluating client outcomes, an understanding of the physiology of cytokines, the occurrences of dysregulation, and the role of cytokines in health and illness is essential. In Part I of this review, cytokine physiology is presented, with an emphasis on characteristics, categories, and mechanism of action. Specific instances of cytokine function in health and disease and implications for nursing research and practice are presented in Part II.
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Inchingolo, Francesco, Angelo Michele Inchingolo, Giuseppina Malcangi, Laura Ferrante, Irma Trilli, Angela Di Noia, Fabio Piras, et al. "The Interaction of Cytokines in Orthodontics: A Systematic Review." Applied Sciences 14, no. 12 (June 13, 2024): 5133. http://dx.doi.org/10.3390/app14125133.
Повний текст джерелаАнотація:
Aim: Cytokines are crucial low-molecular-weight proteins involved in immune responses. This systematic review highlights the need for in-depth studies on cytokines’ biological mechanisms, providing insights into disease onset and potential therapeutic strategies. Materials and methods: A comprehensive literature search identified 18 relevant articles, emphasizing the multifaceted role of cytokines in orthodontic treatment (OT). The quality assessment using the ROBINS-I tool ensures a rigorous evaluation of the included studies, contributing to the overall reliability of the findings. Results and Conclusions: This systematic review explores the intricate relationship between cytokines and OT. Cytokines exhibit different properties, influencing cellular activities through autocrine, paracrine, and endocrine activities. OT, aimed at achieving stable occlusion, induces tension and compression in the periodontal ligament (PDL), triggering cytokine release. Proinflammatory cytokines play a role in inflammation, influencing bone and soft tissue metabolism. Studies show elevated cytokine levels in gingival crevicular fluid (GCF) after orthodontic force application. The choice of orthodontic devices, such as self-ligating brackets, influences cytokine concentrations, indicating the importance of attachment design. Further research promises to enhance orthodontic practices, and optimize patient care.
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Bonner, J. C., and A. R. Brody. "Cytokine-binding proteins in the lung." American Journal of Physiology-Lung Cellular and Molecular Physiology 268, no. 6 (June 1, 1995): L869—L878. http://dx.doi.org/10.1152/ajplung.1995.268.6.l869.
Повний текст джерелаАнотація:
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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Minami, Keita, Yoshiki Yanagawa, Kazuya Iwabuchi, Nobuo Shinohara, Toru Harabayashi, Katsuya Nonomura, and 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, no. 5 (September 1, 2005): 1685–93. http://dx.doi.org/10.1182/blood-2004-12-4738.
Повний текст джерелаАнотація:
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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Tetè, S., D. Tripodi, M. Rosati, F. Conti, G. Maccauro, A. Saggini, E. Cianchetti, et al. "IL-37 (IL-1F7) the Newest Anti-Inflammatory Cytokine Which Suppresses Immune Responses and Inflammation." International Journal of Immunopathology and Pharmacology 25, no. 1 (January 2012): 31–38. http://dx.doi.org/10.1177/039463201202500105.
Повний текст джерелаАнотація:
Cytokines such as interleukins, chemokines and interferons are immunomodulating and inflammatory agents, characterized by considerable redundancy, in that many cytokines appear to share similar functions. Virtually all nucleated cells, but especially epithelial cells and macrophages, are potent producers of cytokines. The objective of this study is to review the detailed mechanism of action and the biological profiles of IL-37, the newest anti-inflammatory cytokine. This review focuses on IL-37, a key cytokine in regulating inflammatory responses, mainly by inhibiting the expression, production and function of proinflammatory cytokines: IL-1 family pro-inflammatory effects are markedly suppressed by IL-37.