Relevant bibliographies by topics / Immunology; Cytokines

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Immunology; Cytokines'

Author: Grafiati
Published: 4 June 2021
Last updated: 4 February 2022

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Journal articles on the topic "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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Dissertations / Theses on the topic "Immunology; Cytokines"

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Palmblad, Karin. "Cytokines and cytokine-directed intervention in experimental arthritis /." Stockholm, 2001. http://diss.kib.ki.se/2001/91-628-4589-6/.

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Ghorayeb, Christine. "The regulation of human B cell effector cytokine profiles by exogenous T helper cell cytokines /." Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111556.

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The Bar-Or laboratory recently reported that human B cells from normal subjects can produce either pro-inflammatory (TNF-alpha; LT) or regulatory (IL-10) effector cytokines depending on their context of activation. It was of interest to investigate the change in B cell cytokine profiles from normal subjects when activated in the context of a Th1 pro-inflammatory environment or a Th2 anti-inflammatory environment. It was found that the B cell regulatory network of effector cytokines from normal subjects is significantly modulated depending on the local cytokine milieu. In addition, it was of interest to study how MS patients' B cell cytokine network would respond in a Th1 pro-inflammatory and a Th2 anti-inflammatory context. It was found that MS patients' B cell cytokine network was dysregulated compared to B cell responses from normal subjects. The findings define a novel regulatory network involving human B cells from normal subjects and point to a newly discovered abnormality in MS patients' B cells.
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Ulfgren, Ann-Kristin. "Cytokines in rheumatoid arthritis /." Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-3823-7/.

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Mundy-Bosse, Bethany L. "Myeloid-Derived Suppressor Cells in Tumor Immunology." The Ohio State University, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=osu1311261626.

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Ahmed, Ahmed Abdelaziz. "Neuroimmune interaction in cutaneous leishmaniasis /." Stockholm, 1998. http://diss.kib.ki.se/search/diss.se.cfm?19980925ahme.

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Diab, Asim Eltayeb. "Experimental bacterial meningitis : studies on immunopathogenesis and immunoregulation /." Stockholm, 1998. http://diss.kib.ki.se/1998/91-628-3008-2.

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Hsieh, Hsiang Chuan. "Checkpoint modulation of T cell immunity by novel fusion cytokines." Thesis, McGill University, 2014. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=121154.

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Functional immunity requires a balanced T cell immune response, which entails the maintenance of de novo production (i.e. TCR repertoire diversity) and the appropriate differentiation of effector subsets at the periphery. However, numerous pathogenic changes can perturb this homeostasis. On the one hand, diminished thymopoiesis or exhausted effectors cause immune dysfunction, leading to the persistence of virally infected or cancerous cells. Unrestrained immune reaction, on the other hand, can cause significant tissue damage. The main objective of my thesis therefore was to develop novel therapeutics to modulate T cell immunity in the context of cancer and inflammatory diseases. Interleukin-7 (IL7) is critically involved in T cell development and homeostatic proliferation. In order to pharmacologically induce T cell neogenesis for immune reconstitution and cancer therapy, we developed a novel biopharmaceutical based on the fusion of GMCSF and IL7 (GIFT7). GIFT7 administration in aged mice led to cortical hyperplasia, effectively reversing tissue involution. GIFT7-mediated hypertrophic effect includes an increase in total thymic cellularity and more importantly a 4-fold increase in the number of CD4-CD8-CD44intCD25-early thymic precursors. In the periphery, GIFT7 selectively expand a CD8+subset from pre-activated T cells with a phenotype defined as CD8+CD44+CD62L+CCR7+KLRG-CD27+, hereafter TGIFT7. The adoptive transfer of OTI-derived CD8 TGIFT7 into OVA-EG7-bearing mice leads to significant tumor regression. Furthermore, the human ortholog of GIFT7 (hGIFT7) leads to a two-fold increase in total cell number after 3 days and >80% of Ki67+expression in both CD4+ and CD8+ PBMC with concurrent reduction in PD1 expression, the cardinal marker of T cell exhaustion. Therapeutically, augmented T cell immunity via GIFT7 delivery rescues mice from disseminated leukemia. On the opposite spectrum of hypofunction, self-directed T cell over-reaction also demands therapeutic intervention. We have previously shown N-terminal modified(tetra-peptide-cleaved) MCP3 possessed immune suppressive activity. In view of this, we hypothesized that a synthetic cytokine linking GMCSF to MCP3 (GMME3) as part of a single polypeptide would augment its immune plasticity. We demonstrated that GMME3 induces significant Ca++ influx, activating IL10+CD21hiCD24hi CD1.dhi subset of splenic B cells (BGMME3) capable of inhibiting antigen presentation and Th17. The adoptive transfer of BGMME3 to mice symptomatic with experimental autoimmune encephalitis attenuated disease progression. Overall, the research presented in this thesis supports the use of GMCSF-based fusion cytokine as novel immune regenerative and modulatory therapeutics to (i)augment thymopoiesis, (ii) promote effector expansion, (iii) and regulate helper polarization. Therefore, our work points to the translational potential of fusion cytokines or fusion-primed immune cells as treatment of T cell dysfunction.
L'immunité fonctionnelle des lymphocytes T exige le maintien de la diversité de répertoire et la différenciation appropriée des sous-ensembles à la périphérie. Cependant, les nombreux changements pathogènes peuvent perturber cette homéostasie. D'une part, la diminution de thymopoïèse ou l'épuisement des effecteurs provoquent un dysfonctionnement immunitaire, conduisant à la persistance des cellules infectées par des virus ou des cellules cancéreuses. Une réaction immunitaire effrénée peut, d'autre part, endommager les tissus. Le principal objectif de ma thèse était donc de développer de nouvelles thérapies pour moduler l'immunité des cellules T dans le contexte du cancer et des maladies inflammatoires. L'interleukine-7 (IL7) est particulièrement importante dans le développement des cellules T et sa prolifération homéostatique. Afin d'induire pharmacologiquement la néogenèse des cellules T, pour la reconstitution immunitaire et le traitement du cancer, nous avons développé un produit biopharmaceutique basé sur la fusion de GM-CSF et IL7 (GIFT7). L'administration de GIFT7 à des souris âgées a conduit à une hyperplasie corticale, inversant efficacement l'involution des tissus. L'effet hypertrophique du GIFT7 provoque une augmentation de la cellularité thymique totale et surtout une multiplication par 4 du nombre de CD4-CD8-CD44intCD25-précurseurs thymiques. Dans la périphérie, GIFT7 provoque la prolifération sélective d'un sous-ensemble CD8+ avec un phénotype défini comme CD8+CD44+CD62L+CCR7+KLRG-CD27+ (TGIFT7). Le transfert adoptif de cellules CD8 dérivée OTI-TGIFT7 dans l'OVA-EG7 des souris porteuses conduit à une régression tumorale significative. En outre, l'orthologue humain de GIFT7(hGIFT7) conduit à une multiplication par deux du nombre de cellules total après 3 jours et > 80% de Ki67+ expression dans les deux CD4+ et CD8+ PBMC avec réduction concomitante de PD1 expression, qui est le marqueur cardinal de l'épuisement des cellules T. L'augmentation de l'immunité des cellules T, via la livraison de GIFT 7, sauve les souris de leucémie diffusée. Sur le spectre opposé d'hypofonction, la sur-réaction de l'auto-cellule T exige également une intervention thérapeutique. Nous avons montré précédemment que le N-terminal modifié (tétra-peptide clivé) MCP3 possédait une activité immunitaire suppressive. Compte tenu de cela, nous avons émis l'hypothèse qu'une cytokine GM-CSF synthétique liée au MCP3 (GMME3) dans le cadre d'un polypeptide unique permettrait d'accroître sa plasticité immunitaire. Nous avons démontré que le GMME3 induit significativement Ca++ afflux, l'activation de l'IL10+CD21hiCD24hiCD1.dhi sous-ensemble de cellules B spléniques (BGMME3) capables d'inhiber la présentation de l'antigène et Th17. Le transfert adoptif de BGMME3 a atténué la progression de la maladie auto-immune de souris présentant des symptômes d'encéphalite expérimentale. Dans l'ensemble, la recherche présentée dans cette thèse soutient l'utilisation de la fusion pour la régénération immunitaire et de la thérapeutique modulation de (i) lathymopoïèse, (ii) l'expansion effecteur, (iii) et de la polarisation d' CD4+. Nos points de travail concernent le potentiel de translation de cytokines de fusion ou de fusion-apprêtées cellules immunitaires pour le traitement de la dysfonction des cellules T.
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Williamson, Eilidh. "Cytokines in the immunopathogenesis of murine graft-versus-host disease." Thesis, University of Glasgow, 1997. http://theses.gla.ac.uk/40906/.

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Murine models of graft-versus-host disease (GvHD) provide important information relevant to clinical bone marrow transplantation (BMT), as well as to other types of T cell-mediated pathology. The nature of the GvHD which develops in (C57BL/6 X DBA/2)F1 (BDF1) mice injected with parental lymphocytes is dependent on whether C57B1/6 (B6) or DBA/2 parental donor cells are used. BDF1 mice injected with B6 donor cells (B6 => BDF1) develop an acute GvHD with early lymphoid hyperplasia and NK cell activation, followed by immunosuppression, activation of anti-host cytotoxic T lymphocytes (CTL), weight loss and early death. In contrast, BDF1 mice given DBA/2 donor cells (DBA/2 => BDF1) exhibit a chronic, stimulatory GvHD, characterised by B cell hyperreactivity, autoantibody production and immune complex-mediated glomerulonephritis (ICGN). Previous studies have shown that the distinct forms of GvHD in BDF1 recipient mice are associated with different patterns of cytokine production. Whereas acute GvHD is characterised by production of high levels of Th1 cytokines, chronic GvHD is associated with a preferential Th2 response. Therefore, it was suggested that the two forms of GvHD may reflect differential activation of distinct subsets of CD4+ T helper (Th) cells. However, when and why such T cell polarisation should occur has remained unclear. A number of recent studies have demonstrated that cytokines produced by cells of the non-specific immune system during the early phase of an immune response can strongly influence the type of specific response which develops subsequently. The main aim of this thesis was to explore the role of these early immune mediators in determining the outcome of the GvHD in BDF1 mice. These studies of the cellular and molecular interactions involved in murine GvHD have implications for understanding the pathogenesis of clinical GvHD and the development of specific therapy following BMT. In addition, they provide an important insight into the regulation of immune responses during other immunologically-mediated diseases.
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Barkhuizen, Mark. "Determination of the role of cytokines using gene deficient mice in African trypanosomiasis infection." Doctoral thesis, University of Cape Town, 2008. http://hdl.handle.net/11427/3119.

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African trypanosomiasis encompasses diseases caused by pathogenic trypanosomes, infecting both humans and animals alike. To determine the immunological role of IL=12 family members in Trypanosoma brucei brucei, Trypanosoma evansi and Trypanosoma congolense infections, IL-12p35¯/¯, IL-12p40¯/¯ and IL-12p35¯/¯/p40¯/¯ mice were used. While the two latter mouse strains lack all IL-12 homologues, IL-12p35¯/¯ mice still produce IL-12p80 homodimers and IL-23. In infection with T.b. brucei and T.evansi; IL-12p35¯/¯, IL-12p40¯/¯ or IL-12p35¯/¯/p40¯/¯ mice were susceptible to both these pathogens, demonstrated by increased mortality compared to wild type C57BL/6 mice. The different IL-12 deficient mouse strains showed similar mortality kinetics, suggesting that IL-12p70 but not the IL-12p80 homodimer or IL-23 plays a crucial role in survival. Similarly, parasitemia control was reduced in the absence of IL-12p70. While plasma levels of IgM and IgG2c were similar between IL-12 deficient mice and wild type mice, IF-γ production. As IFN-γR¯/¯ mice were also highly susceptible to both T.b. brucei and T. evansi, IL-12p70-dependent IFN-γ production seems to be important mechanism involved in resistance against both these pathogens.
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Alshehri, Ali Awadh. "Cell Viability, Cytoskeleton Organization and Cytokines Secretion of RAW 264.7 Macrophages Exposed to Gram-Negative Bacterial Components." Wright State University / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=wright1481857962791924.

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Books on the topic "Immunology; Cytokines"

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1926-, Gerok W., and Gastroenterology Week (1994 : Freiburg-im-Breisgau, Germany), eds. Cytokines and the liver. Dordrecht: Kluwer Academic Publishers, 1995.

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Kelso, Anne. Cytokines in transplantation. Austin: R.G. Landes, 1996.

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Irina, Kiseleva, and SpringerLink (Online service), eds. Mechanical Stretch and Cytokines. Dordrecht: Springer Science+Business Media B.V., 2012.

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service), ScienceDirect (Online, ed. Cytokines and the brain. Amsterdam: Elsevier, 2008.

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Depino, Amaicha Mara. Pro-inflammatory cytokines in learning and memory. Hauppauge, N.Y: Nova Science Publishers, 2010.

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Golding, Basil, and Mahmood Iftekhar. Immunogenicity of therapeutic proteins: Coagulation factors, monoclonal antibodies & cytokines. Rockville, Maryland: Pine House Publishers, 2012.

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Vaddi, Krishna. The chemokine factsbook. San Diego: Academic Press, 1997.

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Cytokines and cytokine receptors. 2nd ed. Oxford: IRL, 1993.

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Balkwill, Frances R. Cytokine molecular biology: A practical approach. 3rd ed. Oxford: Oxford University Press, 2000.

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Cytokines and T lymphocytes: Therapeutic manipulation of the immune system. Austin: R.G. Landes, 1993.

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Book chapters on the topic "Immunology; Cytokines"

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Cruse, Julius M., and Robert E. Lewis. "Cytokines." In Atlas of Immunology, 185–206. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-662-11196-3_10.

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Sam-Yellowe, Tobili Y. "Cytokines." In Immunology: Overview and Laboratory Manual, 117–19. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-64686-8_14.

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Lacy, P., and R. Moqbel. "Eosinophil Cytokines." In Chemical Immunology and Allergy, 134–55. Basel: KARGER, 2000. http://dx.doi.org/10.1159/000058782.

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Sredni-Kenigsbuch, Dvora. "Stress, Immunology, and Cytokines." In Iron Deficiency and Overload, 207–20. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-462-9_12.

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Loppnow, Harald. "Atherosclerosis and Cytokines." In Encyclopedia of Medical Immunology, 79–88. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-0-387-84828-0_178.

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Dokter, W. H. A., and E. Vellenga. "Cytokines and Cell Mediated Immunology." In Immunology and Blood Transfusion, 3–9. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-3094-7_1.

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Chaouat,, Gérard, Nathalie Ledée-Bataille, Karen Bonnet Chea, and Sylvie Dubanchet. "Cytokines and Implantation." In Chemical Immunology and Allergy, 2005, 34–63. Basel: KARGER, 2005. http://dx.doi.org/10.1159/000087820.

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Sudan, Raki. "Cytokines in Cancer Immunotherapy." In Systems and Synthetic Immunology, 255–69. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-3350-1_10.

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Oppenheim, J. J., J. M. Wang, A. W. Lloyd, D. D. Taub, D. J. Kelvin, and R. Neta. "The Cytokine Network: Contributions of Proinflammatory Cytokines and Chemokines." In Progress in Immunology Vol. VIII, 297–304. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-51479-1_39.

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Dahinden, C. A., T. Brunner, M. Krieger, S. C. Bischoff, and A. L. de Weck. "Cytokines in allergic inflammation." In Progress in Immunology Vol. VIII, 411–18. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-51479-1_54.

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Conference papers on the topic "Immunology; Cytokines"

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Kroon, Sanne, Kaitlin Dempsey, Margherita Boieri, and Shawn Demehri. "Abstract B102: Epithelium-derived cytokines in breast carcinogenesis." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 17-20, 2019; Boston, MA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm19-b102.

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Sachdeva, Mohit, Beatriz Aranda-Orgilles, Philippe Duchateau, Laurent Poirot, and Julien Valton. "Abstract A60: GM-CSF modulation restricts the secretion of main cytokines associated with CAR T-cell induced cytokine release syndrome." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 17-20, 2019; Boston, MA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm19-a60.

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Franks, Elizabeth, Etienne Melese, Bryant Harbourne, Liz Halvorsen, Rachel Cederberg, Jenna Collier, Natalie Firmino, et al. "Abstract A38: Oncogenes drive production of immunosuppressive cytokines to facilitate lung cancer progression." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 27-30, 2018; Miami Beach, FL. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm18-a38.

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Islam, Mirazul, Elsa Haniffah Mohamed, Ezalia Esa, Nor Rizan Kamaluddin, Shamsul Mohd Zain, Yuslina Yusoff, Yassen Assenov, Zahurin Mohamed, and Zubaidah Zakaria. "Abstract B86: Circulating cytokines, chemokines, and small molecules follow distinct expression patterns in acute myeloid leukemia." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; October 1-4, 2017; Boston, MA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/2326-6074.tumimm17-b86.

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Dubauskaite, Jolanta, Laura Bradshaw, Ashley Merlino, Xianhui Rong, Connie Gee, Glenn Dranoff, and Maria Pinzon-Ortiz. "Abstract B79: Proinflammatory cytokine profile of syngeneic models." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 27-30, 2018; Miami Beach, FL. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm18-b79.

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Eissmann, Moritz, Christine Dijkstra, and Matthias Ernst. "Abstract PR015: IL33 cytokine signalling in gastrointestinal cancers - a therapy target?" In Abstracts: AACR Virtual Special Conference: Tumor Immunology and Immunotherapy; October 19-20, 2020. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/2326-6074.tumimm20-pr015.

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Wongkajornsilp, Adisak, Nathawadee Sawatpiboon, Sunisa Duangsa-ard, Kanda Kasetsinsombat, Kittipong Maneechotesuwan, and Suradej Hongeng. "Abstract A39: Cholangiocarcinoma-exposed cytokine-induced killer cells developed senescence and exhaustion." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; October 20-23, 2016; Boston, MA. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/2326-6074.tumimm16-a39.

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Havunen, Riikka, Suvi Parviainen, Mikko Siurala, and Akseli Hemminki. "Abstract B07: Characterization of T-cell therapy enhancing oncolytic adenoviruses with human cytokine expression." In Abstracts: AACR Special Conference: Tumor Immunology and Immunotherapy: A New Chapter; December 1-4, 2014; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/2326-6074.tumimm14-b07.

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Jackson, Christopher M., Wikum Dinalankara, John Choi, Thomas R. Nirschl, Christina M. Kochel, Ayush Pant, Denis Routkevitch, et al. "Abstract A32: Characterizing patterns of cytokine coexpression with immune checkpoint markers in CD4 and CD8 tumor-infiltrating lymphocytes." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 17-20, 2019; Boston, MA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm19-a32.

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Miyahira, Andrea K., Diana L. Simons, Frederick Dirbas, Ellie Guardino, Shruti Sheth, Robert Carlson, and Peter P. Lee. "Abstract A51: Identification of cytokine network signaling abnormalities in immune cells from cancer patients." In Abstracts: AACR Special Conference on Tumor Immunology: Multidisciplinary Science Driving Basic and Clinical Advances; December 2-5, 2012; Miami, FL. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.tumimm2012-a51.

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