Journal articles: 'Immunology; Cytokines'

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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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Koval, H. D., O. M. Yuzko, and A. I. Kurchenko. "RELATION OF Th1, Th2, Treg, Th17 CYTOKINES OF PERITONEAL FLUID IN WOMEN WITH ENDOMETRIOSIS, ASSOCIATED WITH INFERTILITY." Immunology and Allergy: Science and Practice, no. 4 (December 23, 2019): 43–50. http://dx.doi.org/10.37321/immunology.2019.04-06.

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Endometriosis is one of the leading diseases of the female reproductive organs and is the cause of almost a third of all cases of female infertility. It has been suggested that in women with endometriosis associated with infertility, the levels, nature of production and the ratio of cytokines of cells of different profiles in the peritoneal fluid change, which may play a pathogenetic role (to promote the development of immune inflammation of a certain type) in the development of the disease itself infertility. Aim of the study: to determine the features of the ratio of Th1, Th2, Treg, Th17 cytokines of peritoneal fluid in women with endometriosis associated with infertility. Materials and methods: The study group included 58 women who were diagnosed with external genital endometriosis, namely: peritoneal form and infertility for at least 2 years. The control group consisted of 30 women with tubal genital infertility. No other pathological process, at the time of observation, was detected in control patients. The study was conducted at the Center for Infertility Treatment (Chernivtsi) from 2009 to 2015, following the concept of informed consent of the patient to conduct research and other ethical principles in relation to persons who are the object of the study. Peritoneal fluid was collected during laparoscopy during the proliferative phase of the menstrual cycle. Cytokine levels were determined by enzyme-linked immunosorbent assay (ELISA). The results of the study. The cytokine profile in the peritoneal fluid of women with infertility-associated endometriosis is characterized by an increase in levels of IL-2, TNF-α, IL-6, IL-17, IL-10, IL-18. The largest proportion of all cytokines under study in the peritoneal fluid is IL-10 (28%), followed by IL-2, IL-6 and IL-18 in the order of decreasing relative amount (16%, 14% and 13%, respectively). respectively. The TGF-β (7%) was then placed in relative weight reduction. TNF-α and IL-17 6% each; IL-12 (4%); IL-1β and INF-γ are 3% percent each. The lowest proportion, as in the peripheral blood, was IL-4, which was incomplete 1 percent. The total relative number of cytokines Th1 is 25%, cytokines Th2 – incomplete 15%, cytokines Treg cells – 35%, cytokines Th 17 – IL-17 is 6% and cytokines produced mainly by macrophages and killer cells – 20%. Thus, the total ratio of Th1/Th2 cytokines in women with endometriosis was 2.5:1.5. Conclusions: In the peritoneal fluid, pronounced changes in the cytokine profile are observed, significantly prevail over changes in the peripheral blood, and are characterized by the growth of IL-2 (p <0.001), TNF-α (p <0.001), INF-γ (p <0.001), IL -6 (p <0.001), IL-17 (p <0.001), IL-10 (p <0.001), TGF-β (p <0.05), IL-12 (p <0.001), IL-18 (p <0.001). Local production is characterized by a 2.45-fold decrease in the Th1/Th2 cytokine ratio, which indicates a predominance of the Th2-mediated immune response.

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Hafler, David A. "Cytokines and interventional immunology." Nature Reviews Immunology 7, no. 6 (June 2007): 423. http://dx.doi.org/10.1038/nri2101.

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Yuriev, Serhii. "Assessment of the cytokine profile in patients with allergic rhinitis caused by sensitization to house dust mite." Immunology and Allergy: Science and Practice, no. 1 (April 8, 2020): 25–31. http://dx.doi.org/10.37321/immunology.2020.01-04.

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The aim of the study was to evaluate the serum cytokine profile of patients with allergic rhinitis (AR) sensitized to house dust mites and to establish their role in the regulation of IgE synthesis Materials and Methods. The study included 60 patients with AR at the age of 20-60. According to the level of total IgE (IgE>100 kU/L), patients were divided into two groups with an IgE-dependent and IgE-independent form of AR. In the study, the serum levels of IL-2, g-IFN, IL-4, IL-5, IL-13, IL-10 and TGF-b in the blood serum were determined by ELISA. Results. According to the study, it was found that patients with an IgE-dependent form of AR are characterized by a decrease in the level of Th1 cytokines IL-2 and g-IFN, an increase in the level of Th2 cytokines – IL-4, IL-5 and IL-13 and a decrease in Treg cytokines – IL-10 and TGF- b. At the same time, a significant decrease in the level of inhibiting cytokine IL-10 was established in comparison with the group of patients with an IgE-independent form of AR. For patients with an IgE-independent form, only elevated levels of IL-13 were found. No significant differences were found between other Th1 and Th2 and Treg cytokines. Conclusions. The study showed that in patients with AR sensitization to house dust mites, IL-13 acts as a key cytokine in the IgE-independent form of AR, which can be important in the future for both predicting and treating AR.

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Arsentieva, N. A., and Areg A. Totolian. "METHODOLOGICAL ISSUES OF DETERMINING CONCENTRATIONS OF SOME CYTOKINES IN PERIPHERAL MBLOOD FROM HEALTHY INDIVIDUALS." Medical Immunology (Russia) 20, no. 5 (November 6, 2018): 763–74. http://dx.doi.org/10.15789/1563-0625-2018-5-763-774.

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Cytokines are the most important factors in pathogenesis of infectious, allergic, autoimmune, lymphoproliferative diseases and immunopathological processes. Many cytokines are very useful therapeutic targets for immunodiagnostics of different human diseases. Measurement of the cytokine levels by immunochemical methods in various biological fluids is usually used for diagnostic evaluation. Content analysis of research articles from two Russian immunological journals, “Meditsinskaya Immunologiya” = “Medical Immunology (Russia)” and “Infektsiya i immunitet” = “Russian Journal of Infection and Immunity,”, shows that ELISA, xMAP multiplex immunoassay, and CBA technologies are the most common methods used in clinical and immunological studies aimed for determination of cytokine contents in blood serum/plasma. Normal ranges of some plasma/serum cytokines in healthy individuals were subject to wide variations when using different methods and specific reagents from various manufacturers. The normal ranges applied by the CBA-technology, are significantly higher than appropriate values obtained by ELISA or xMAP-technologies. Most studies included a small control group, usually limited by 15-20 persons. In most of these works, blood serum samples were used for assays, whereas EDTA-conserved plasma was taken only in few studies. It has been concluded that the results of cytokine measurements in blood serum/plasma in healthy individuals vary in wide ranges, and depend on many factors, e.g., initial sampling material, mode of technology, type of test systems, and characteristics of the group under study: number of patients, age, gender, geographical factor, etc. The mentioned data demonstrate a need for large-scale multicenter clinical studies, in order to standardize measurements of the cytokine levels in human peripheral blood and to specify their normal values.

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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.

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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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Asthana, Deshratn, and Mary Ann Fletcher. "Cytokines and chemokines in clinical immunology." Clinical Immunology Newsletter 17, no. 5 (May 1997): 61–62. http://dx.doi.org/10.1016/s0197-1859(97)82491-0.

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Norlander, Allison E., Meena S. Madhur, and David G. Harrison. "The immunology of hypertension." Journal of Experimental Medicine 215, no. 1 (December 15, 2017): 21–33. http://dx.doi.org/10.1084/jem.20171773.

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Although systemic hypertension affects a large proportion of the population, its etiology remains poorly defined. Emerging evidence supports the concept that immune cells become activated and enter target organs, including the vasculature and the kidney, in this disease. Mediators released by these cells, including reactive oxygen species, metalloproteinases, cytokines, and antibodies promote dysfunction of the target organs and cause damage. In vessels, these factors enhance constriction, remodeling, and rarefaction. In the kidney, these mediators increase expression and activation of sodium transporters, and cause interstitial fibrosis and glomerular injury. Factors common to hypertension, including oxidative stress, increased interstitial sodium, cytokine production, and inflammasome activation promote immune activation in hypertension. Recent data suggest that isolevuglandin-modified self-proteins in antigen-presenting cells are immunogenic, promoting cytokine production by the cells in which they are formed and T cell activation. Efforts to prevent and reverse immune activation may prove beneficial in preventing the long-term sequelae of hypertension and its related cardiovascular diseases.

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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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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.

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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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Xue, Diyuan, Eric Hsu, Yang-Xin Fu, and Hua Peng. "Next-generation cytokines for cancer immunotherapy." Antibody Therapeutics 4, no. 2 (April 1, 2021): 123–33. http://dx.doi.org/10.1093/abt/tbab014.

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Abstract Most studies focus on the first and second signals of T cell activation. However, the roles of cytokines in immunotherapy are not fully understood, and cytokines have not been widely used in patient care. Clinical application of cytokines is limited due to their short half-life in vivo, severe toxicity at therapeutic doses, and overall lack of efficacy. Several modifications have been engineered to extend their half-life and increase tumor targeting, including polyethylene glycol conjugation, fusion to tumor-targeting antibodies, and alteration of cytokine/cell receptor-binding affinity. These modifications demonstrate an improvement in either increased antitumor efficacy or reduced toxicity. However, these cytokine engineering strategies may still be improved further, as each strategy poses advantages and disadvantages in the delicate balance of targeting tumor cells, tumor-infiltrating lymphocytes, and peripheral immune cells. This review focuses on selected cytokines, including interferon-α, interleukin (IL)-2, IL-15, IL-21, and IL-12, in both preclinical studies and clinical applications. We review next-generation designs of these cytokines that improve half-life, tumor targeting, and antitumor efficacy. We also present our perspectives on the development of new strategies to potentiate cytokine-based immunotherapy.

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Balkwill, F. R. "Cytokines in Hemopoiesis, Oncology, and Immunology III." British Journal of Cancer 73, no. 5 (March 1996): 711. http://dx.doi.org/10.1038/bjc.1996.124.

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Lacy, Paige, and Jennifer L. Stow. "Cytokine release from innate immune cells: association with diverse membrane trafficking pathways." Blood 118, no. 1 (July 7, 2011): 9–18. http://dx.doi.org/10.1182/blood-2010-08-265892.

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AbstractCytokines released from innate immune cells play key roles in the regulation of the immune response. These intercellular messengers are the source of soluble regulatory signals that initiate and constrain inflammatory responses to pathogens and injury. Although numerous studies describe detailed signaling pathways induced by cytokines and their specific receptors, there is little information on the mechanisms that control the release of cytokines from different cell types. Indeed, the pathways, molecules, and mechanisms of cytokine release remain a “black box” in immunology. Here, we review research findings and new approaches that have begun to generate information on cytokine trafficking and release by innate immune cells in response to inflammatory or infectious stimuli. Surprisingly complex machinery, multiple organelles, and specialized membrane domains exist in these cells to ensure the selective, temporal, and often polarized release of cytokines in innate immunity.

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Brennan, F. M. "Cytokines." Immunology Today 12, no. 2 (February 1991): 96. http://dx.doi.org/10.1016/0167-5699(91)90170-x.

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Hirano, Toshio. "Cytokines." Immunology Today 13, no. 7 (January 1992): 281. http://dx.doi.org/10.1016/0167-5699(92)90014-x.

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Bendtzen, Klaus. "Cytokines and natural regulators of cytokines." Immunology Letters 43, no. 1-2 (December 1994): 111–23. http://dx.doi.org/10.1016/0165-2478(94)00153-7.

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Robertson, Sarah A., Mats Brännström, and Robert F. Seamark. "Cytokines in rodent reproduction and the cytokine-endocrine interaction." Current Opinion in Immunology 4, no. 5 (January 1992): 585–90. http://dx.doi.org/10.1016/0952-7915(92)90031-9.

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Whiteside, T. L. "Cytokines and cytokine measurements in a clinical laboratory." Clinical and diagnostic laboratory immunology 1, no. 3 (1994): 257–60. http://dx.doi.org/10.1128/cdli.1.3.257-260.1994.

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Lloyd, Andrew R., and Jim Johnston. "Cytokines and cytokine receptors in health and disease." Cytokine 5, no. 5 (September 1993): 399–406. http://dx.doi.org/10.1016/1043-4666(93)90029-5.

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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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Aksu, Serap. "Single Cell Interrogation using Optofluidic Platforms for Systems Immunology." MRS Advances 1, no. 56 (2016): 3783–88. http://dx.doi.org/10.1557/adv.2016.337.

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ABSTRACTThe main objective of this report is to demonstrate novel engineering technologies to investigate regulatory mechanisms of systems immunology in a time-dependent and high-throughput manner. Understanding of immune system behavior is crucial for accurate prognosis of infections and identification of diseases at early stage. An ultimate goal of biomedical engineering is to develop predictive models of immune system behavior in tissue, which necessitates a comprehensive map of dynamic (time-dependent) input-output relationships at the individual cell level. Traditionally, biochemical analysis on the cell signaling is obtained from bulky cell ensembles which average over relevant individual cell response. The response consists firstly of signaling protein (cytokine) secretions which are released during a disease state and which are used to activate the immune system to respond to the disease. We investigate the cytokine secretion dynamics of a single immune cell in response to the stimulant using automated and comprehensive optofluidic platforms. These platforms enable survival and manipulation of single cells in compartments having compatible sizes with cells as well as provide precise control over the type, dose and time-course of the stimulant. The cytokine secretion dynamics of single cell are typically explained by measuring the types, rates, frequencies and concentrations of various cytokines. For the quantitative measurements, label free localized surface plasmon resonance (LSPR) based biosensor can be integrated within the microfluidic device. Microfluidic channels can confine secreted cytokines in compartments, minimize dilution effects and increase detection sensitivity for label free plasmonic biosensing. The direct application of LSPR to in-situ live cell function analysis is still in its infancy and use of such in-situ, real time, and label free biodetection will effortlessly provide high-throughput quantitative bioanalysis for understanding immune system behavior.

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Nelson, Robert P., and Mark Ballow. "26. Immunomodulation and immunotherapy: Drugs, cytokines, cytokine receptors, and antibodies." Journal of Allergy and Clinical Immunology 111, no. 2 (February 2003): S720—S732. http://dx.doi.org/10.1067/mai.2003.146.

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Yan, Chen, Le Yu, Xiu-Ling Zhang, Jing-Jing Shang, Jie Ren, Jie Fan, Xue-Qin Feng, Rong-Wei Zhang, Zhong-Bin Xia, and Xin-Wang Duan. "Cytokine Profiling in Chinese SLE Patients: Correlations with Renal Dysfunction." Journal of Immunology Research 2020 (October 9, 2020): 1–8. http://dx.doi.org/10.1155/2020/8146502.

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Background. Systemic lupus erythematosus (SLE) is a chronic, systemic autoimmune disease that commonly causes kidney damage. Therefore, we measured plasma levels of cytokines that may be related to renal dysfunction in SLE patients. Methods. To explore the differences between SLE patients with renal dysfunction and healthy volunteers, the levels of cytokines in plasma were screened using a human cytokine antibody array. Then, we chose fourteen of the elevated cytokines for verification with an expanded sample size by a human magnetic Luminex assay. Plasma samples were isolated from SLE patients (n=72) and healthy volunteers (n=8). Results. Cytokine antibody array data showed elevated plasma cytokines in SLE patients with renal dysfunction compared with healthy volunteers. By using the human magnetic Luminex assay, we found that plasma levels of CHI3L1, GDF-15, IGFBP-2, MIF, ST2, TFF3, and uPAR were significantly higher in SLE patients than in healthy volunteers. Plasma levels of CXCL4 were significantly lower in the active group than in the inactive group, and plasma levels of CHI3L1, IGFBP-2, MIF, and MPO were significantly higher in the active group than in the inactive group. We also analyzed the correlation between plasma cytokine levels and the SLEDAI-2K, and our results showed that the plasma levels of the fourteen selected cytokines were weakly correlated or not correlated with the SLEDAI-2K. We further analyzed the correlation between cytokines and renal dysfunction. Plasma levels of GDF-15 and TFF3 were highly positively correlated with serum creatinine levels and 24-hour urine protein levels. Conclusion. Our data suggest that plasma levels of GDF-15 and TFF3 are potential renal dysfunction markers in SLE patients, but plasma levels of these cytokines are not correlated with the SLEDAI-2K. Further study is warranted to determine how these cytokines regulate inflammatory responses and renal dysfunction in SLE.

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Lieberman, Jay A., Anna-Barbara Moscicki, Jan L. Sumerel, Yifei Ma, and Mark E. Scott. "Determination of Cytokine Protein Levels in Cervical Mucus Samples from Young Women by a Multiplex Immunoassay Method and Assessment of Correlates." Clinical and Vaccine Immunology 15, no. 1 (October 31, 2007): 49–54. http://dx.doi.org/10.1128/cvi.00216-07.

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ABSTRACT Cytokines in cervical mucus are likely to play important roles in controlling pathogens. The cervical mucosal environment is complex, however, with many endogenous and exogenous factors that may affect cytokine levels. We used a multiplex, suspension-array-based immunoassay method to measure 10 proinflammatory (interleukin-1β [IL-1β], IL-6, and IL-8) and immunoregulatory (gamma interferon [IFN-γ], IL-2, IL-4, IL-5, IL-10, IL-12, and IL-13) cytokines in cervical mucus specimens collected via ophthalmic sponge from 72 healthy, nonpregnant women and correlate their levels with biologic and behavioral covariates in a cross-sectional design. Proinflammatory and immunoregulatory cytokines were readily detected, although proinflammatory cytokines were present at markedly higher levels than were immunoregulatory cytokines. Among the covariates examined, the most striking finding was the significant (P ≤ 0.05) association between depressed levels of the cytokines IFN-γ, IL-1β, IL-6, and IL-10 and cigarette smoking. Also, nonsignificant trends toward lower cytokine levels were found in the settings of incident and persistent human papillomavirus infection. The ready detection of proinflammatory cytokines may be reflective of the female genital tract as an anatomic site that is constantly exposed to immunogenic stimulation. Cigarette smoking appears to downregulate cytokine responses in the cervical mucosa, which may help explain the implicated role of tobacco use as a cofactor for cervical cancer development.

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Honey, Karen. "Overactive cytokines." Nature Reviews Immunology 4, no. 1 (January 2004): 6. http://dx.doi.org/10.1038/nri1286.

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Al-Banna, Nadia, Raj Raghupathy, and M. John Albert. "Correlation of Proinflammatory and Anti-Inflammatory Cytokine Levels with Histopathological Changes in an Adult Mouse Lung Model of Campylobacter jejuni Infection." Clinical and Vaccine Immunology 15, no. 12 (September 30, 2008): 1780–87. http://dx.doi.org/10.1128/cvi.00193-08.

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ABSTRACT Campylobacter jejuni is a major cause of diarrhea in humans. A mouse lung model of infection was previously established for C. jejuni. We used this model to study cytokine production in the lungs and correlated it with pathological changes. C. jejuni strain 81-176 or sterile phosphate-buffered saline was intranasally inoculated into adult BALB/c mice. The levels of proinflammatory cytokines (gamma interferon, tumor necrosis factor alpha, interleukin-1β [IL-1β], IL-2) and anti-inflammatory cytokines (IL-4, IL-10), in addition to those of IL-6, were assessed on days 1, 3, and 5 postinfection by enzyme-linked immunosorbent assay, and the ratios of proinflammatory cytokines to anti-inflammatory cytokines were calculated. Since IL-6 is unique in that it is both a proinflammatory cytokine and a TH2 cytokine, it was considered to be both in the determination of these ratios. The significance of the cytokine levels and ratios were determined by the Mann-Whitney U test (P ≤ 0.05). The induction of proinflammatory cytokines in the lungs of infected mice, as indicated by the cytokine levels and ratios, coincided with the accumulation of neutrophils and activated macrophages, in addition to the clearance of the bacterial load and bacteriumlike structures that we have previously shown in the same groups of mice. This was followed by increased levels of anti-inflammatory cytokines and the resolution of inflammation and pathology in the lungs. This study demonstrates the dynamics of cytokine production and their correlation with tissue inflammation and the resolution of infection. This model is useful for further studies of the pathogenesis of C. jejuni infection and vaccine evaluation.

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Harber, Mark, Anette Sundstedt, and David Wraith. "The role of cytokines in immunological tolerance: potential for therapy." Expert Reviews in Molecular Medicine 2, no. 9 (November 27, 2000): 1–20. http://dx.doi.org/10.1017/s1462399400002143.

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Current immunosuppression protocols, although often effective, are nonspecific and therefore hazardous. Consequently, immunological tolerance that is antigen specific and does not globally depress the patient's immune system has become one of the Holy Grails of immunology. Since the discovery that cytokines have immunomodulatory effects, extensive research has investigated the potential of these molecules to induce and maintain specific immunological tolerance in the context of transplantation, allergy and autoimmunity. In this article, we review the possible mechanisms by which cytokines can modulate the immune response and the animal models that frequently confound the theory that a single cytokine, or group of cytokines, can induce tolerance in a predictable manner. Finally, we discuss the role of cytokines at a paracrine level, particularly in the context of inducing and maintaining antigen-specific, regulatory T cells with the clinical potential to suppress specific immune responses.

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Gankovskaya, L. V., L. S. Namazova-Baranova, G. V. Poriadin, V. V. Grechenko, V. A. Gankovsky, A. A. Alekseeva, Zh M. Salmashi, A. N. Kazimirsky, B. G. Bragvadze, and O. A. Svitich. "CHANGES OF INNATE IMMUNITY INDEXES IN SEVERE ASTHMA IN CHILDREN." Medical Immunology (Russia) 21, no. 1 (January 24, 2019): 99–106. http://dx.doi.org/10.15789/1563-0625-2019-1-99-106.

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At the present time, the role of innate immunity in pathogenesis of bronchial asthma (BA) is actively studied, in particular, significance of TLRs and cytokines. The study included 42 patients with severe bronchial asthma (from 3 to 12 years old), and 67 healthy children at the same age. Expression of TLR2, TLR4, and TLR9 genes was evaluated by PCR-RT from the scrapings of nasal mucosa; cytokines (IL-33, TSLP, IL-4, TGF-β1 and IL-28B) were assayed in nasal swabs by ELISA technique. The main results were as follows: an increased gene expression of TLR2, TLR4, TLR9 genes was revealed in the nasal mucosa scraps from the patients with bronchial asthma as compared to healthy children. We have also measured the contents of important cytokines secreted by the respiratory epithelium in the course of TLRs activation. The study of IL-33, TSLP, IL-4 in nasal samples revealed significantly increased concentrations of these cytokines in the patients with severe BA against the control group. A study of TGF-βlevels in nasal cavity swabs revealed a significant decrease of this regulatory cytokine in the group of pediatric patients with asthma. Worth of note, evaluation of antiviral IL-28B cytokine in the group of patients with severe BA showed a significant downward trend, in comparison to the control indexes. Hence, one may conclude on some disturbances of local innate immunity system in the patients with severe BA which manifest as hyperexpression of TLRs genes, increased production of proinflammatory and epithelial cytokines, decreased production of antiviral IL-28B cytokine, and TGF-β1.

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Parkhouse, Michel R. E. "Cytokines." Veterinary Immunology and Immunopathology 35 (February 1993): 114–26. http://dx.doi.org/10.1016/0165-2427(93)90141-p.

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Miyake, S., H. Yagita, T. Maruyama, H. Hashimoto, N. Miyasaka, and K. Okumura. "Beta 1 integrin-mediated interaction with extracellular matrix proteins regulates cytokine gene expression in synovial fluid cells of rheumatoid arthritis patients." Journal of Experimental Medicine 177, no. 3 (March 1, 1993): 863–68. http://dx.doi.org/10.1084/jem.177.3.863.

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Inflammatory cytokines have been implicated in the pathogenesis of rheumatoid arthritis (RA), whereas the mechanisms for constitutive production of inflammatory cytokines in affected joints are largely unknown. Recently, integrin-mediated interaction with extracellular matrix (ECM) proteins has been demonstrated to play a role in regulating cytokine production in T cells and monocytes. In this study, we investigated the contribution of the beta 1 integrin-mediated interaction with ECM proteins to the persistent cytokine gene expression in RA synovial fluid mononuclear cells (SFMNC). We examined mRNA expression of 14 cytokines in the SFMNC of three RA patients, which were either fresh or cultured overnight in serum-free medium on ECM-coated plates, by polymerase chain reaction with a panel of oligonucleotide primers specific for each cytokine. The persistent expression of various cytokine mRNA found in fresh SFMNC was maintained after overnight culture in serum-free medium on ECM proteins, especially on laminin (LM), but not on serum albumin. This effect of LM was inhibited by an anti-integrin beta 1 chain (CD29) mAb, as well as by an anti-CD3 mAb, indicating an important role of the beta 1 integrin-mediated interaction with ECM proteins in regulating persistent cytokine gene expression in RA SFMNC, and a key role of T cells in regulating inflammatory monokine production.

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Blakemore, Alexandra I. F. "Cytokines." Cytokine 3, no. 4 (July 1991): 360. http://dx.doi.org/10.1016/1043-4666(91)90506-9.

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Vijayaraghava, Ambarish, and Venkatesh Doreswamy. "Exercise and the cytokines-interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α): A review." Annals of Medical Physiology 1, no. 1 (April 8, 2017): 3–8. http://dx.doi.org/10.23921/amp.2017v1i1.263485.

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Interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were one of the first few cytokines to be discovered. The normative data for levels of cytokines IL-6 and TNF-α in particular and all other cytokines in general have not yet been established well. The normal levels for each of the cytokines vary from one race to another. Therefore, all studies need to be done in cases and controls belonging to the same race or same populations. The kits for cytokine assays are expensive and running the assays is laborious and time consuming. It is recommended that the serum/plasma samples are run in duplicates and triplicates to avoid error. Immunology and the field of cytokines is an area which has many domains unexplored. As yet, it is not clearly understood by what mechanisms and pathways each of the cytokines alter the levels of other cytokines. Exercise or physical activity is an intervention which can be administered easily and levels of cytokines measured before and after intervention in same individuals taking all the above mentioned factors into consideration. Hence it is imperative that we look into studies on exercise and cytokines to do further research in the field of cytokines.

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Lévesque, J. P., D. I. Leavesley, S. Niutta, M. Vadas, and P. J. Simmons. "Cytokines increase human hemopoietic cell adhesiveness by activation of very late antigen (VLA)-4 and VLA-5 integrins." Journal of Experimental Medicine 181, no. 5 (May 1, 1995): 1805–15. http://dx.doi.org/10.1084/jem.181.5.1805.

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Cytokines are known to be important regulators of normal hemopoiesis, acting in concert with components of the bone marrow microenvironment. Interactions with this microenvironment are known to regulate the proliferation, differentiation, and homing of hemopoietic progenitor (CD34+) cells. Adhesive interactions with the extracellular matrix retain CD34+ cells in close proximity to cytokines, but may also provide important costimulatory signals. Thus, the functional states of adhesion receptors are critical properties of CD34+ cells, but the physiological mechanisms responsible for regulating functional properties of cell adhesion receptors on primitive hemopoietic cells are still unknown. We confirm that the integrins very late antigen (VLA)-4 and VLA-5 are expressed on the CD34+ cell lines MO7e, TF1, and on normal bone marrow CD34+ progenitor cells, but in a low affinity state, conferring on them a weak adhesive phenotype on fibronectin (Fn). Herein, we show that the cytokines interleukin (IL)-3, granulocyte-macrophage CSF (GM-CSF), and KIT ligand (KL) are physiological activators of VLA-4 and VLA-5 expressed by MO7e, TF1, and normal bone marrow CD34+ progenitor cells. Cytokine-stimulated adhesion on Fn is dose dependent and transient, reaching a maximum between 15 and 30 min and returning to basal levels after 2 h. This cytokine-dependent activation is specific for VLA-4 and VLA-5, since activation of other beta 1 integrins was not observed. The addition of second messenger antagonists staurosporine and W7 abolished all cytokine-stimulated adhesion to Fn. In contrast, genistein inhibited KL-stimulated adhesion, but failed to inhibit GM-CSF- and IL-3-stimulated adhesion. Our data suggest that cytokines GM-CSF and IL-3 specifically stimulate beta 1 integrin function via an "inside-out" mechanism involving protein kinase activity, while KL stimulates integrin activity through a similar, but initially distinct, pathway via the KIT tyrosine-kinase. Thus, in addition to promoting the survival, proliferation, and development of hemopoietic progenitors, cytokines also regulate adhesive interactions between progenitor cells and the bone marrow microenvironment by modifying the functional states of specific integrins. These data are of importance in understanding the fundamental processes of beta 1 integrin activation and cellular response to mitogenic cytokines as well as on the clinical setting where cytokines induce therapeutic mobilization of hematopoietic progenitors.

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Olbei, Marton, John P. Thomas, Isabelle Hautefort, Agatha Treveil, Balazs Bohar, Matthew Madgwick, Lejla Gul, Luca Csabai, Dezso Modos, and Tamas Korcsmaros. "CytokineLink: A Cytokine Communication Map to Analyse Immune Responses—Case Studies in Inflammatory Bowel Disease and COVID-19." Cells 10, no. 9 (August 29, 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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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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Davies, Kristen, Kamran Mirza, Jessica Tarn, Nadia Howard-Tripp, Simon J. Bowman, Dennis Lendrem, and Wan-Fai Ng. "Fatigue in primary Sjögren’s syndrome (pSS) is associated with lower levels of proinflammatory cytokines: a validation study." Rheumatology International 39, no. 11 (June 27, 2019): 1867–73. http://dx.doi.org/10.1007/s00296-019-04354-0.

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Abstract Primary Sjögren’s syndrome (pSS) is a chronic autoimmune rheumatic disease with symptoms including dryness, fatigue, and pain. The previous work by our group has suggested that certain proinflammatory cytokines are inversely related to patient-reported levels of fatigue. To date, these findings have not been validated. This study aims to validate this observation. Blood levels of seven cytokines were measured in 120 patients with pSS from the United Kingdom Primary Sjögren’s Syndrome Registry and 30 age-matched healthy non-fatigued controls. Patient-reported scores for fatigue were classified according to severity and compared to cytokine levels using analysis of variance. The differences between cytokines in cases and controls were evaluated using Wilcoxon test. A logistic regression model was used to determine the most important identifiers of fatigue. Five cytokines, interferon-γ-induced protein-10 (IP-10), tumour necrosis factor-α (TNFα), interferon-α (IFNα), interferon-γ (IFN-γ), and lymphotoxin-α (LT-α) were significantly higher in patients with pSS (n = 120) compared to non-fatigued controls (n = 30). Levels of two proinflammatory cytokines, TNF-α (p = 0.021) and LT-α (p = 0.043), were inversely related to patient-reported levels of fatigue. Cytokine levels, disease-specific and clinical parameters as well as pain, anxiety, and depression were used as predictors in our validation model. The model correctly identifies fatigue levels with 85% accuracy. Consistent with the original study, pain, depression, and proinflammatory cytokines appear to be the most powerful predictors of fatigue in pSS. TNF-α and LT-α have an inverse relationship with fatigue severity in pSS challenging the notion that proinflammatory cytokines directly mediate fatigue in chronic immunological conditions.

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Davila, Jennifer G., Mauro P. Avanzi, Francine Goldberg, and W. Beau Mitchell. "The Immunologic Role of Platelets in Sickle Cell Disease Pathophysiology." Blood 120, no. 21 (November 16, 2012): 1015. http://dx.doi.org/10.1182/blood.v120.21.1015.1015.

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Abstract Abstract 1015 Introduction: Platelets are mediators of inflammation as well as thrombosis. Platelets are necessary for normal inflammation and play a primary role in the immune clearance of certain pathogens. Platelets secrete cytokines when they are activated, and can also synthesize proteins de novo when activated, such as IL-1b. Sickle Cell Disease (SCD) is characterized by an activated immune system, and it is now recognized that much of the pathology of SCD results from an inflammatory vasculopathy. Platelets may mediate some of the vascular injury through their inflammatory function, as indicated by: 1) elevated platelet counts in SCD, 2) platelets circulating in an activated state in SCD, as judged by activation dependent surface markers, and 3) elevated blood levels of platelet derived inflammatory proteins, such as soluble CD40 ligand. Hypothesis: A direct mechanism through which platelets could impact the immune system in SCD would be to produce and secrete cytokines. We hypothesized that the identity profile and quantity of cytokines produced and secreted by platelets would be altered in SCD compared to controls, and that those alterations would be associated with clinical status. We measured the expression levels of cytokine mRNA in resting and activated platelets in patients with SCD and compared those to controls. We also measured thrombin-induced secretion of cytokines from highly purified platelets in buffer and compared that to controls. Cytokines representing TH1, TH2, and TH17 immune phenotypes were measured. Methods: Whole blood was collected from adult patients with SCD undergoing exchange transfusions. Platelets were isolated by sequential centrifugation followed by passage through an affinity column for glycophorin-A and CD45. Platelets were activated with 0.125U/ml thrombin for 18 hours in M199 medium at 37C, and then the supernatant (the platelet releasate) was analyzed for cytokine content. Cytokines were measured using BD Cytometric Bead Array for Th1/Th2/Th17 profile: IL-1β (driver of inflammation, secreted from platelets), IL-2, IL-4, IL-6 (induction/maintenance of autoimmunity), IL-10, IL-17a (maintenance of autoimmunity), TNF-α, IFN-γ, and sCD40L (secreted from platelets). Total RNA was isolated from either fresh platelets or platelets after activation and analyzed by QRT-PCR. Relative mRNA quantity was measured using certified mRNA primer sets and SYBR green detector, using β-actin as an internal control. Results: Both IL-6 and TGFβ mRNA levels were significantly increased to more than nine- and six-fold over control levels, respectively. IL-1β and IL-10 mRNA levels were also increased over controls, but this did not reach significance. Platelet secretion of IL-6, IL-1β, and soluble CD40 ligand was increased approximately 300-, 21-, and 5-fold, respectively, in sickle cell platelets compared to controls. The alterations of cytokine mRNA and cytokine secretion were more pronounced in patients with alloantibodies than in those without. These preliminary findings support the idea of platelets as active modulators of SCD inflammation, and indicate a novel mechanism through which antiplatelet agents may be beneficial in SCD. Disclosures: No relevant conflicts of interest to declare.

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Zhang, Minghuang, Theresa Caragine, Haichao Wang, Pamela S. Cohen, Galina Botchkina, Kuniyasu Soda, Marina Bianchi, et al. "Spermine Inhibits Proinflammatory Cytokine Synthesis in Human Mononuclear Cells: A Counterregulatory Mechanism that Restrains the Immune Response." Journal of Experimental Medicine 185, no. 10 (May 19, 1997): 1759–68. http://dx.doi.org/10.1084/jem.185.10.1759.

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The local production of proinflammatory cytokines mediates the host response to inflammation, infection, and injury, whereas an overexpression of these mediators can injure or kill the host. Recently, we identified a class of multivalent guanylhydrazone compounds that are effective inhibitors of proinflammatory cytokine synthesis in monocytes/macrophages. The structure of one such cationic molecule suggested a molecular mimicry with spermine, a ubiquitous endogenous biogenic amine that increases significantly at sites of inflammation and infection. Here, we addressed the hypothesis that spermine might counterregulate the innate immune response by downregulating the synthesis of potentially injurious cytokines. When spermine was added to cultures of human peripheral blood mononuclear cells stimulated with lipopolysaccharide (LPS), it effectively inhibited the synthesis of the proinflammatory cytokines tumor necrosis factor (TNF), interleukin-1 (IL-1), IL-6, MIP-1α, and MIP-1β. The inhibition of cytokine synthesis was specific and reversible, with significant inhibition of TNF synthesis occurring even when spermine was added after LPS. The mechanism of spermine-mediated cytokine suppression was posttranscriptional and independent of polyamine oxidase activity. Local administration of spermine in vivo protected mice against the development of acute footpad inflammation induced by carrageenan. These results identify a distinct molecular counterregulatory role for spermine in downregulating the monocyte proinflammatory cytokine response.

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Romani, Nikolaus, Eckhart Kämpgen, Franz Koch, Christine Heufler, and Gerold Schuler. "Dendritic Cell Production of Cytokines and Responses to Cytokines." International Reviews of Immunology 6, no. 2-3 (January 1990): 151–61. http://dx.doi.org/10.3109/08830189009056626.

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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.

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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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Kleiner, Giulio, Annalisa Marcuzzi, Valentina Zanin, Lorenzo Monasta, and Giorgio Zauli. "Cytokine Levels in the Serum of Healthy Subjects." Mediators of Inflammation 2013 (2013): 1–6. http://dx.doi.org/10.1155/2013/434010.

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Growing knowledge about the cytokine network response has led to a better comprehension of mechanisms of pathologies and to the development of new treatments with biological drugs, able to block specific molecules of the immune response. Indeed, when the cytokine production is deregulated, diseases often occur. The understanding of the physiological mechanism of the cytokine network would be useful to better comprehend pathological conditions. Moreover, since the immune system and response change their properties with development, differences in patients' age should be taken into account, both in physiological and in pathological conditions. In this study, we analyzed the profile of 48 cytokines and chemokines in the serum of healthy subjects, comparing adults (≥18 years) with young children and children (1–6 and 7–17 years). We found that a certain number of cytokines were not being produced in healthy subjects; others showed a constant serum level amongst the groups. Certain cytokines exhibited a downward or an upward trend with increasing age. The remaining cytokines were up- or downregulated in the group of the children with respect to the other groups. In conclusion, we drew some kinds of guidelines about the physiological production of cytokines and chemokines, underling the difference caused by aging.

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Zhang, X., L. Giangreco, H. E. Broome, C. M. Dargan, and S. L. Swain. "Control of CD4 effector fate: transforming growth factor beta 1 and interleukin 2 synergize to prevent apoptosis and promote effector expansion." Journal of Experimental Medicine 182, no. 3 (September 1, 1995): 699–709. http://dx.doi.org/10.1084/jem.182.3.699.

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The signals that determine the size and duration of the primary T cell immune response are not well defined. We studied CD4 T cells at an important checkpoint in their development: when they have become effectors and are ready to rapidly mediate effector functions, both via direct interaction with antigen (Ag)-presenting cells and via cytokine production. We determined the effects of specific Ag and the cytokines interleukin (IL) 2 and transforming growth factor (TGF) beta 1 on T helper cell type 2 (Th2) effector apoptosis versus expansion. Th2-polarized effector cells were generated in vitro from naive CD4 T of T cell receptor transgenic mice, and then restimulated with or without peptide Ag plus Ag-presenting cells and cytokines. In the absence of added cytokines, effector cells cultured without Ag died of apoptosis after 4-7 d. Paradoxically, Ag both induced proliferation and high levels of cytokine synthesis and accelerated effector cell death. IL-2 directly induced proliferation of effectors, supported and prolonged Ag-induced proliferation, and partially blocked apoptosis. TGF-beta did not effect proliferation or influence cytokine secretion, but it also partially blocked apoptosis. Together, IL-2 and TGF-beta synergized to almost completely block apoptosis, resulting in prolonged effector expansion and leading to the accumulation of a large pool of specific effectors. When Ag and both cytokines were present, the effector population increased 10(4)-10(5) fold over 20 d of culture. The synergy of IL-2 and TGF-beta suggests that they interfere with programmed cell death by distinct mechanisms. Since Th2 effectors are specialized to help B cells develop into antibody-secreting plasma cells, these results suggest that the availability of Ag and of the cytokines IL-2 and TGF-beta is a key factor influencing the fate of Th2 effector cells and thus the size and duration of the primary antibody response.

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Goel, G., A. J. M. Daveson, C. E. Hooi, J. A. Tye‐Din, S. Wang, E. Szymczak, L. J. Williams, et al. "Serum cytokines elevated during gluten‐mediated cytokine release in coeliac disease." Clinical & Experimental Immunology 199, no. 1 (October 2019): 68–78. http://dx.doi.org/10.1111/cei.13369.

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Saukkonen, K., S. Sande, C. Cioffe, S. Wolpe, B. Sherry, A. Cerami, and E. Tuomanen. "The role of cytokines in the generation of inflammation and tissue damage in experimental gram-positive meningitis." Journal of Experimental Medicine 171, no. 2 (February 1, 1990): 439–48. http://dx.doi.org/10.1084/jem.171.2.439.

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Cytokines mediate many host responses to bacterial infections. We determined the inflammatory activities of five cytokines in the central nervous system: TNF-alpha, IL-1 alpha, IL-1 beta, macrophage inflammatory protein 1 (MIP-1), and macrophage inflammatory protein 2 (MIP-2). Using a rabbit model of meningeal inflammation, each cytokine (except IL-1 beta) induced enhanced blood brain barrier permeability, leukocytosis in cerebrospinal fluid, and brain edema. Homologous antibodies to each mediator inhibited leukocytosis and brain edema, and moderately decreased blood brain barrier permeability. In rabbits treated with anti-CD-18 antibody to render neutrophils dysfunctional for adhesion, each cytokine studied lost the ability to cause leukocytosis and brain edema. After intracisternal challenge with pneumococci, antibodies to TNF or IL-1 prevented inflammation, while anti-MIP-1 or anti-MIP-2 caused only a 2-h delay in the onset of inflammation. We suggest these cytokines have multiple inflammatory activities in the central nervous system and contribute to tissue damage during pneumococcal meningitis.

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Kannanganat, Sunil, Bill G. Kapogiannis, Chris Ibegbu, Lakshmi Chennareddi, Paul Goepfert, Harriet L. Robinson, Jeffrey Lennox, and Rama Rao Amara. "Human Immunodeficiency Virus Type 1 Controllers but Not Noncontrollers Maintain CD4 T Cells Coexpressing Three Cytokines." Journal of Virology 81, no. 21 (August 29, 2007): 12071–76. http://dx.doi.org/10.1128/jvi.01261-07.

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ABSTRACT Here, we evaluate the cytokine coexpression profiles of human immunodeficiency virus (HIV)-specific CD4 T cells for the expression of the cytokines gamma interferon (IFN-γ), interleukin-2, and tumor necrosis factor alpha. In controllers, CD4 T cells producing three or two cytokines (triple producers and double producers, respectively) represented >50% of the total response. In contrast, in noncontrollers ∼75% of responding cells produced only one cytokine (single producers), mostly IFN-γ. Cells producing three cytokines were functionally superior to those producing single cytokines and showed an inverse correlation (P < 0.001) with viral load. These results demonstrate a strong association between the maintenance of highly functional CD4 T cells producing three cytokines and control of HIV-1.

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Vossen, Ann C. T. M., and Huub F. J. Savelkoul. "Cytokines in Clinical and Experimental Transplantation." Mediators of Inflammation 3, no. 6 (1994): 403–10. http://dx.doi.org/10.1155/s0962935194000566.

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Allograft rejection is a complex process, which requires interactions between different cell types and a variety of soluble factors, such as cytokines. In this review we discuss the role of cytokines in the induction and effector phases of the rejection process and in the induction and maintenance of allospecific graft tolerance. Furthermore, we discuss the feasibility of clinical graft function monitoring by measuring cytokines and the possibilities for intervention in the cytokine network in order to inhibit graft rejection and eventually obtain graft acceptance.

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Bianchi, M., O. Bloom, T. Raabe, P. S. Cohen, J. Chesney, B. Sherry, H. Schmidtmayerova, et al. "Suppression of proinflammatory cytokines in monocytes by a tetravalent guanylhydrazone." Journal of Experimental Medicine 183, no. 3 (March 1, 1996): 927–36. http://dx.doi.org/10.1084/jem.183.3.927.

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An overproduction of proinflammatory cytokines by activated macrophages/monocytes mediates the injurious sequelae of inflammation, septic shock, tissue injury, and cachexia. We recently synthesized a tetravalent guanylhydrazone compound (CNI-1493) that inhibits cytokine-inducible arginine transport and nitric oxide (NO) production in macrophages, and protects mice against lethal endotoxemia and carrageenan-induced inflammation. During these investigations we noticed that CNI-1493 effectively prevented lipopolysaccharide (LPS)-induced NO production, even when added in concentrations 10-fold less than required to competitively inhibit L-arginine uptake, suggesting that the suppressive effects of this guanylhydrazone compound might extend to other LPS-induced responses. Here, we report that CNI-1493 suppressed the LPS-stimulated production of proinflammatory cytokines (tumor necrosis factor [TNF], interleukins 1beta and 6, macrophage inflammatory proteins 1alpha and 1beta) from human peripheral blood mononuclear cells. Cytokine suppression was specific, in that CNI-1493 did not inhibit either the constitutive synthesis of transforming growth factor beta or the upregulation of major histocompatibility complex class II by interferon gamma (IFN-gamma). In contrast to the macrophage suppressive actions of dexamethasone, which are overridden in the presence of IFN-gamma, CNI-1493 retained its suppressive effects even in the presence of IFN-gamma. The mechanism of cytokine-suppressive action by CNI-1493 was independent of extracellular L-arginine content and NO production and is not restricted to induction by LPS. As a selective inhibitor of macrophage activation that prevents TNF production, this tetravalent guanylhydrazone could be useful in the development of cytokine-suppressive agents for the treatment of diseases mediated by overproduction of cytokines.

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Zanetta, Jean-Pierre, Christelle Cebo, and Gérard Vergoten. "Lectin Activities of Cytokines: A New Concept in Immunology." Trends in Glycoscience and Glycotechnology 14, no. 79 (2002): 303–18. http://dx.doi.org/10.4052/tigg.14.303.

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Sigal, Leonard H. "Molecular Biology and Immunology for Clinicians, 10 Cytokines-1." JCR: Journal of Clinical Rheumatology 5, no. 6 (December 1999): 360–62. http://dx.doi.org/10.1097/00124743-199912000-00012.

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Spriewald, Bernd M., J. Stephen Billing, and Kathryn J. Wood. "Cytokines as mediators in immunologic tolerance." Current Opinion in Organ Transplantation 6, no. 1 (March 2001): 7–13. http://dx.doi.org/10.1097/00075200-200103000-00002.

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Journal articles on the topic 'Immunology; Cytokines'

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