Готові списки джерел за темами / Immunometabolism, T cells, autoimmunity

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Добірка наукової літератури з теми "Immunometabolism, T cells, autoimmunity"

Автор: Grafiati
Опубліковано: 11 березня 2023

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Статті в журналах з теми "Immunometabolism, T cells, autoimmunity"

1

Gallucci, Stefania, Marita Chakhtoura, Michael H. Lee, and Connie C. Qiu. "The metabolic modulator metformin affects the activation and survival of murine dendritic cell subsets." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 180.17. http://dx.doi.org/10.4049/jimmunol.202.supp.180.17.

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Abstract Unique immunometabolic pathways control the ability of dendritic cell subsets to activate, and metabolic modulators are proposed as therapeutic candidates in cancer and autoimmunity, although their effects on specific immune cells are not fully known. The metabolic inhibitor metformin, the first-choice oral treatment for type II diabetes, has many effects on immunometabolism, including the inhibition of complex I of oxidative phosphorylation. Metformin was shown to decrease the severity of autoimmunity in murine models by inhibiting the activation of T cells. Moreover, it can diminish tumor growth through affecting the polarization of tumor-infiltrating macrophages. Here, we determined the effects of metformin on three subsets of dendritic cells that are proposed to have different energy requirements for activation. Upon TLR stimulation, we found that metformin does not affect the activation of the inflammatory GM-CSF-dependent dendritic cells (iDCs) or the Flt3-L-dependent conventional dendritic cells (cDCs), which rely on an immuno-metabolic shift to glycolysis to fully activate and express costimulatory molecules and pro-inflammatory cytokines, but it decreased cDC survival at resting state. In contrast, we found that metformin inhibited the activation of plasmacytoid dendritic cells (pDCs), which requires both an increase in oxidative phosphorylation and glycolysis for activation. Our studies provide a new layer of complexity in the potential of metformin as treatment in autoimmunity and cancer by showing that this drug can inhibit the activation of pDCs and also eliminate resting cDCs, therefore altering in opposite directions the impact of these innate cell subsets on the immune response.
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Wu, R., J. An, T. Ding, H. Xue, X. F. Li, and C. Wang. "POS0396 THE LEVEL OF PERIPHERAL REGULATORY T CELLS IS ASSOCIATED WITH THE CHANGES OF INTESTINAL MICROBIOTA IN PATIENTS WITH RHEUMATOID ARTHRITIS." Annals of the Rheumatic Diseases 80, Suppl 1 (May 19, 2021): 427–28. http://dx.doi.org/10.1136/annrheumdis-2021-eular.2783.

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Background:Rheumatoid arthritis (RA) is a systemic autoimmunity inflammation disease characterized with chronic aggressive arthritis and the presence of abnormal antibodies. Several observations showed that the breakdown of immune tolerance caused by many complex interactions was involved in the development of RA[1]. However, the pathogenesis of RA remained unclear. It has been confirmed that the imbalance of Th17 and Treg cells play a crucial role in destroying immune tolerance [2]. Besides, researches showed that intestinal microbiota can influence host immunity by acting on the immune cells to play pro-inflammatory or anti-inflammatory effect, and in turn immune system can also regulate the microbiota[3, 4]. Thus, a frontier point of view in the field of rheumatism, immune microecology, was proposed, which is a novel concept for the breakdown of immune tolerance. Studies have confirmed that there was an imbalance of intestinal microbiota in patients with RA [4]. But the relationship between the CD4+T subsets cells and intestinal microbiota in RA is unknown.Objectives:We detected and compared the absolute number of CD4+T cells subsets in the peripheral blood and the proportion or abundance of intestinal microbiota in patients with RA and healthy adults, and then analyzed the relationship between them to explore the role of CD4+T cells subsets and intestinal microbiota in the pathogenesis of RA.Methods:We collected the sample of stool and blood from 15 patients with RA hospitalized at the Second Hospital of Shanxi Medical University and 8 age and gender-matched healthy controls(HC). The absolute number of CD4+T cells subsets including Th1, Th2, Th17 and Treg cells were detected by flow cytometry. The 16S rRNA in the stool specimens were sequenced by the Roche/45 high-throughput sequencing platform. We analyzed whether there was correlarion between CD4+T subsets cells and intestinal microbiota.Results:Patients with RA had a higher level of Christensenellaceae and a lower level of Pseudomonadaceae as compared with those of HCs at the family level (p<0.05). And at the genus level, the patients with RA had higher levels of Ruminococcus torques, Christensenellaceae R-7, Ruminiclostridium 9 and Ruminococcus 1 compared with those of HCs (p<0.05) (Figure 1).And the Ruminococcus torques at the genus level was negative correlated with the absolute number of Treg cells (p<0.001) (Figure 2).Conclusion:The results here suggested that there were different proportion or abundance of intestinal microbiota between the patients with RA andHCs. And the changes of intestinal microbiota such as Ruminococcus torques were associated with Treg cells, further indicating that the imbalance of intestinal microbiota in RA can destory the immune tolerance. The above results uncovered that the intestinal microbiota had immunomodulatory function, which may be the upstream mechanism participated in the pathogenesis of RA.References:[1]Weyand CM, Goronzy JJ. The immunology of rheumatoid arthritis. Nat Immunol 2021, 22(1): 10-18.[2]Weyand CM, Goronzy JJ. Immunometabolism in the development of rheumatoid arthritis. Immunol Rev 2020, 294(1): 177-187.[3]Brown EM, Kenny DJ, Xavier RJ. Gut Microbiota Regulation of T Cells During Inflammation and Autoimmunity. Annu Rev Immunol 2019, 37: 599-624.[4]du Teil Espina M, Gabarrini G, Harmsen HJM, Westra J, van Winkelhoff AJ, van Dijl JM. Talk to your gut: the oral-gut microbiome axis and its immunomodulatory role in the etiology of rheumatoid arthritis. FEMS Microbiol Rev 2019, 43(1).Figure 1.At the family level (a-b) and the genus level(c-f), the relative abundance of intestinal microbiota in patients with RA and HCs were different. Data were expressed as median (Q1, Q3) and analyzed by Wilcoxon test. (*** P < 0.001, **P < 0.01 and *P < 0.05).Figure 2.A heatmap shows the correlation between the intestinal microbiota and CD4+T cells in patients with RA, and Ruminococcus torques at the genus level was negative related with Treg cells. (Colors indicate the Spearman rank correlation, *** P < 0.001).Disclosure of Interests:None declared
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Newton, Ryan, Bhavana Priyadharshini, and Laurence A. Turka. "Immunometabolism of regulatory T cells." Nature Immunology 17, no. 6 (May 19, 2016): 618–25. http://dx.doi.org/10.1038/ni.3466.

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Chia, Tzu-yi, Andrew Zolp, and Jason Miska. "Polyamine Immunometabolism: Central Regulators of Inflammation, Cancer and Autoimmunity." Cells 11, no. 5 (March 5, 2022): 896. http://dx.doi.org/10.3390/cells11050896.

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Polyamines are ubiquitous, amine-rich molecules with diverse processes in biology. Recent work has highlighted that polyamines exert profound roles on the mammalian immune system, particularly inflammation and cancer. The mechanisms by which they control immunity are still being described. In the context of inflammation and autoimmunity, polyamine levels inversely correlate to autoimmune phenotypes, with lower polyamine levels associated with higher inflammatory responses. Conversely, in the context of cancer, polyamines and polyamine biosynthetic genes positively correlate with the severity of malignancy. Blockade of polyamine metabolism in cancer results in reduced tumor growth, and the effects appear to be mediated by an increase in T-cell infiltration and a pro-inflammatory phenotype of macrophages. These studies suggest that polyamine depletion leads to inflammation and that polyamine enrichment potentiates myeloid cell immune suppression. Indeed, combinatorial treatment with polyamine blockade and immunotherapy has shown efficacy in pre-clinical models of cancer. Considering the efficacy of immunotherapies is linked to autoimmune sequelae in humans, termed immune-adverse related events (iAREs), this suggests that polyamine levels may govern the inflammatory response to immunotherapies. This review proposes that polyamine metabolism acts to balance autoimmune inflammation and anti-tumor immunity and that polyamine levels can be used to monitor immune responses and responsiveness to immunotherapy.
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Griffiths, Christopher E. M., and John J. Voorhees. "Psoriasis, T Cells and Autoimmunity." Journal of the Royal Society of Medicine 89, no. 6 (June 1996): 315–19. http://dx.doi.org/10.1177/014107689608900604.

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Beer, W. E., and C. M. E. Rowland Payne. "Psoriasis, T Cells and Autoimmunity." Journal of the Royal Society of Medicine 89, no. 10 (October 1996): 600. http://dx.doi.org/10.1177/014107689608901035.

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Vila, Josephine, John D. Isaacs, and Amy E. Anderson. "Regulatory T cells and autoimmunity." Current Opinion in Hematology 16, no. 4 (July 2009): 274–79. http://dx.doi.org/10.1097/moh.0b013e32832a9a01.

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Beissert, Stefan. "T cells in cutaneous autoimmunity." Experimental Dermatology 12, no. 6 (December 2003): 916. http://dx.doi.org/10.1111/j.0906-6705.2003.0156f.x.

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Tsai, S., A. Shameli, and P. Santamaria. "CD8+ T cells in Autoimmunity." Inmunología 27, no. 1 (January 2008): 11–21. http://dx.doi.org/10.1016/s0213-9626(08)70045-3.

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Crispin, Jose C., Maria Ines Vargas, and Jorge Alcocer-Varela. "Immunoregulatory T cells in autoimmunity." Autoimmunity Reviews 3, no. 2 (February 2004): 45–51. http://dx.doi.org/10.1016/s1568-9972(03)00086-7.

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Дисертації з теми "Immunometabolism, T cells, autoimmunity"

1

Tänzer, Aline. "Molecular Mechanisms of Immunometabolic Dysfunction in Multiple Sclerosis." Doctoral thesis, Humboldt-Universität zu Berlin, 2019. http://dx.doi.org/10.18452/20482.

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Multiple Sklerose (MS) ist eine chronische neuro-degenerative Erkrankung des zentralen Nervensystems, die durch auto-immun-bedingte Prozesse charakterisiert ist. T Zellen wurden als wesentliche pro-inflammatorische Mediatoren mit der Pathogenese der MS assoziiert. In gesunden Individuen passen Immunzellen ihren Metabolismus, wie die mitochondriale Atmung und Glykolyse, ihrer jeweiligen Funktion und ihrem inflammatorischen Phänotyp an. Im Krankheitsverlauf der MS ist die Bedeutung der metabolischen Anpassung und der damit verbundenen pro-inflammatorischen Mechanismen von T Zell-Subpopulationen noch nicht eindringlich erforscht. Um dieser Fragestellung nachzugehen wurden Relapsing Remitting MS (schubförmig, RRMS) Patienten und sorgfältig aufeinander abgestimmte gesunde Kontrollprobanden als Teil der Studie Depression und Immunfuktion bei MS rekrutiert (n=62). Den Patienten und gesunden Kontrollprobanden wurde Nüchternblut entnommen, woraus periphäre mononukleäre Blutzellen (PBMC) aufgearbeitet wurden, um anschließend CD4+ und CD8+ T Zellen zu isolieren. Die erzielten Ergebnisse zeigten CD4+ T Zell-spezifische Verringerungen der mitochondrialen Atmung und glykolytischen Aktivität in der MS Patienten Kohorte im Vergleich zur Kohorte der gesunden Kontrollprobanden. Darüberhinaus wurden, zusätzlich zu den umfangreichen phänotypischen Charakterisierungen der PBMCs via Durchflußzytometrie, erhöhte Werte des mitochondrialen Membranproteins CPT1a in CD4+ T Zell-Subpopulationen in der MS Patienten Kohorte detektiert. Die Analyse der CD4+ CD25- CD127+ konventionellen T Zell- Subpopulation ergab leicht erniedrigte Werte von IL7-Rα in MS Patienten. Genexpressionsanalysen, die mit pro-inflammatorischen und metabolischen Genen assoziiert sind, ergaben keine Veränderungen in den T Zell-Subpopulationen der MS Patienten. Die in dieser Studie erzielten Ergebnisse weisen auf Funktionsstörungen bei der metabolischen Anpassung in T-Zell-Subpopulationen bei MS Patienten hin und helfen, den Beitrag des Immunmetabolismus bei der Pathogenese der MS Erkrankung besser zu verstehen.
Multiple Sclerosis (MS) is a chronic neurodegenerative disease of the central nervous system characterized by autoimmune-mediated mechanisms. T cells have been associated as central pro-inflammatory mediators in MS pathogenesis. In healthy individuals, immune cells adapt metabolic programs like mitochondrial respiration and glycolysis based on their function and inflammatory phenotype. However, the relevance of metabolic reprogramming and associated pro-inflammatory mechanisms in T cell subpopulations in MS disease is not well understood yet. To address this question, Relapsing Remitting MS (RRMS) patients and meticulously matched healthy control (HC) participants were recruited as part of the clinical study Depression and Immune Function in MS (n=62). Blood samples, after a period of fasting, were collected and CD4+ and CD8+ T cells isolated from peripheral blood mononuclear cells (PBMC). The results obtained demonstrated decreased mitochondrial and glycolytic activity specific to CD4+ T cells in the MS patient cohort compared to the HC participant cohort. Furthermore, increased CPT1a mitochondrial membrane protein levels were detected in CD4+ T cell subpopulations in the MS patient cohort as assessed in comprehensive flow cytometry PBMC phenotype investigations. The analysis of the CD4+ CD25- CD127+ conventional T cell subpopulation moreover revealed a trend of decreased IL7-Rα expression levels in MS patients. Gene expression measurements of pro-inflammatory and metabolic genes did not reveal alterations in MS patients’ T cell subpopulations. The results obtained in this study allude to dysfunctions in metabolic reprogramming in T cell subpopulations in MS patients and help to better understand the contribution of immunometabolism in the pathogenesis of MS disease.
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May, Kenneth F. "T cell costimulation in anti-tumor immunity and autoimmunity." Connect to this title online, 2004. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1085004772.

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Анотація:
Thesis (Ph. D.)--Ohio State University, 2004.
Document formatted into pages; contains xv, 178 p. Includes bibliographical references. Abstract available online via OhioLINK's ETD Center; full text release delayed at author's request until 2006 May 20.
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Chen, Yuling [Verfasser]. "Immunometabolism of inflamm-aging in naive and memory CD4+ T cells / Yuling Chen." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2019. http://d-nb.info/120204333X/34.

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Thompson, Angus Gordon. "Dendritic cell NFkB function in T cell activation and autoimmunity /." [St. Lucia, Qld.], 2004. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe18273.pdf.

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Zancanaro, Krauss Maria Eduarda. "CD4+ T cell metabolism during Trichuris muris infection." Thesis, University of Manchester, 2018. https://www.research.manchester.ac.uk/portal/en/theses/cd4-t-cell-metabolism-during-trichuris-muris-infection(24eb0cc7-db70-46ea-ba49-e4fe3d5a5d03).html.

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Trichuris trichiura is a gastrointestinal dwelling nematode that infects almost 500 million people worldwide. T. muris occurs naturally in mice and is very closely related the human whipworm, making it a suitable model to dissect the immune response against the parasite. Studies using the Trichuris muris system have identified CD4+ T cells as dictators of the outcome of infection. In wild type mice, infection with a high dose of T. muris eggs leads to resistance and worm expulsion, which are dependent on a Th2 response and the secretion of type 2 cytokines especially interleukin (IL) 13. Chronicity is dependent on a Th1 response and occurs when mice are infected with a low dose of T. muris eggs. It is well established that metabolic changes are essential to promoting T cell activation and effector function. Moreover, during chronic infection the host immune system is continuously exposed to parasite antigen, which represents a metabolic challenge. This thesis has investigated the importance of T cell metabolism during response against T. muris. Data presented here show that low and high dose T. muris infections promote upregulation of the glycolytic pathway in CD4+ T cells. During later stages of chronic infection, CD4+ T cells displayed supressed glycolysis and mitochondrial respiration, and may be due to metabolic modulation imposed by the parasite. Leucine uptake via the amino acid transporter Slc7a5 was previously shown to be required for mTORC1 activation and for T cell effector function. Data presented here show that in early stages following a high dose T. muris infection, mice that lack Slc7a5 in T cells have delayed worm expulsion, impaired production of antibodies, and lower levels of IL-13. Their CD4+ T cells present reduced glycolytic rates when compared to cells from cohoused infected wild type mice. However, at later stages of infection, antibody, IL-13 and glycolytic levels were restored together with worm expulsion. CD4+ T cells from the early stage of infection showed reduced phosphorylation of mTOR, which suggested that impairment of function was mTOR dependent. Indeed, mice lacking mTOR in T cells fail to expel a high dose of parasites. They showed abrogation of IL-13 production, impairment in antibody class switching and their CD4+ T cells failed to upregulate glycolysis. Thus, this thesis shows that mTOR is essential for the proper functioning of T cells during T. muris infection and efficient amino acid transport plays a significant role. Taken together, these data show that metabolic orchestration of T cell function influences the capacity to effectively control helminth infection and that even subtle changes in T cell metabolic control can have a major effect on response phenotype.
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Kissler, Stephan. "How transgenic T cells interpret encounter with peptide antigen." Thesis, University of Bristol, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.324380.

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Ratts, Robert Bruce. "The role of chronically stimulated and senscent T cells in autoimmunity." Access limited to abstract only until after 9/25/2007, 2006. http://www4.utsouthwestern.edu/library/ETD/etdDetails.cfm?etdID=ETD#206.

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Amorim, Garcia da Rosa Catarina Alexandre. "The role of regulatory T cells in the prevention of autoimmunity." Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312209.

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Lee, Priscilla. "Defining pathways that promote and characterize pathogenic T cells in CNS autoimmunity." The Ohio State University, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=osu1448984666.

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Colamatteo, Alessandra. "Metabolic control of FoxP3 expression in human regulatory T cells." Doctoral thesis, Universita degli studi di Salerno, 2017. http://hdl.handle.net/10556/2686.

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Анотація:
2015 - 2016
Regulatory CD4+CD25+ T (Treg) cells play a central role in the maintenance of immune self-tolerance and homeostasis. Although Treg cells operate through multiple mechanisms, it appears that the expression of the transcription factor Forkhead-box-P3 (FoxP3) is crucial for their function. Here we describe human peripheral Treg (pTreg) cells that develop from CD4+CD25- T (Tconv) cells following suboptimal stimulation via the T cell antigen receptor (TCR). This population of pTreg cells, which we call inducible Treg (iTreg) cells, is characterized by high FoxP3 expression, strong suppressive capacity and an active proliferative and metabolic state. The development of iTreg cells tightly depends on glycolysis, which controls FoxP3 splicing variants containing exon 2 (FoxP3-E2), through the glycolytic enzyme enolase-1. Remarkably, iTreg cells suppressive activity is impaired in autoimmune diseases such as relapsing remitting multiple sclerosis (RR-MS), and associates with the reduction of FoxP3-E2 expression, secondarily to impaired glycolysis and IL-2/IL-2R/STAT-5 signalling. These results suggest a novel mechanism that links glucose metabolism to the induction of specific FoxP3 splicing variants, via enolase-1, that directly impact on human Treg cell function, in health and in autoimmunity. [edited by author]
Le cellule T regolatorie CD4+CD25+ (Treg) svolgono un ruolo centrale nel mantenimento dell’omeostasi e della tolleranza immunitaria. Sebbene le cellule Treg operino attraverso diversi meccanismi, sembra che l'espressione del fattore di trascrizione Forkhead-box-P3 (FoxP3) è fondamentale per la loro funzione. Qui descriviamo le cellule Treg periferiche (pTreg) umane che si sviluppano dalle cellule T CD4+CD25- (Tconv) dopo stimolazione subottimale del recettore delle cellule T (TCR). Questa popolazione di cellule pTreg, chiamata cellule Treg indotte (iTreg), è caratterizzata da un'elevata espressione di FoxP3, da una forte capacità soppressoria e da uno stato proliferativo e metabolico attivo. Lo sviluppo delle cellule iTreg dipende fortemente dalla glicolisi, che controlla le varianti di splicing di FoxP3 contenenti l'esone 2 (FoxP3-E2), attraverso l'enzima glicolico enolasi-1. In particolare, l’attività soppressoria delle cellule iTreg è compromessa nelle malattie autoimmuni come la sclerosi multipla recidivante-remittente (RR-MS) e si associa alla riduzione dell'espressione di FoxP3-E2, secondariamente alla compromissione della glicolisi e della via di segnalazione IL-2 / IL-2R / STAT-5. Questi risultati suggeriscono un nuovo meccanismo che collega il metabolismo del glucosio all'induzione di specifiche varianti di splicing di FoxP3, attraverso l'enolasi-1, che ha un impatto diretto sulla funzionalità delle cellule Treg, sia in condizioni fisiologiche che in corso di autoimmunità. [a cura dell'autore]
XXIX n.s.
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Книги з теми "Immunometabolism, T cells, autoimmunity"

1

Zanetti, M. Memory T cells. New York: Springer Science+Business Media, 2010.

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Memory T cells. New York: Springer Science+Business Media, 2010.

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3

L, Adorini, ed. Immunointervention in autoimmunity by Th1/Th2 regulation. New York: Springer, 1997.

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4

Andras, Perl, ed. Autoimmunity: Methods and protocols. Totowa, N.J: Humana Press, 2004.

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Autoimmunity: Methods and protocols. 2nd ed. New York: Humana Press, 2012.

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6

W, Alt Frederick, and Vogel Henry J. 1920-, eds. Molecular mechanisms of immunological self-recognition. San Diego: Academic Press, 1993.

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7

N, Crispe I., ed. T lymphocytes in the liver: Immunobiology, pathology, and host defense. New York: Wiley-Liss, 1999.

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8

Andrzej, Mackiewicz, Kurpisz Maciej, and Żeromski Jan 1938-, eds. Progress in basic and clinical immunology. New York: Kluwer Academic/Plenum Publishers, 2001.

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Andrzej, Mackiewicz, Kurpisz Maciej, Żeromski Jan 1938-, and European Immunology Meeting (14th : 2000 : Poznań, Poland), eds. Progress in basic and clinical immunology. New York: Kluwer Academic/Plenum Publishers, 2001.

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10

R, Bock Gregory, Goode Jamie, and Novartis Foundation, eds. Generation and effector functions of regulatory lymphocytes. Chichester: John Wiley, 2003.

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Частини книг з теми "Immunometabolism, T cells, autoimmunity"

1

Land, Walter Gottlieb. "Immunometabolism of Dendritic Cells and T Cells." In Damage-Associated Molecular Patterns in Human Diseases, 837–44. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-78655-1_35.

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Weyand, Cornelia M., Ewa Bryl, and Jörg J. Goronzy. "The Role of T Cells in Rheumatoid Arthritis." In Autoimmunity, 183–95. Dordrecht: Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-010-0981-2_13.

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Milone, Michael C. "Car T Cells for Autoimmunity." In Hematopoietic Stem Cell Transplantation and Cellular Therapies for Autoimmune Diseases, 26–32. Boca Raton: CRC Press, 2021. http://dx.doi.org/10.1201/9781315151366-4.

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Forouhi, Nita, Sandra M. McLachlan, Shirley L. Middleton, Marian Atherton, Peter H. Baylis, Fred Clark, and Bernard Rees Smith. "Thyroglobulin Autoantibody IgG Subclasses; Regulation By T Cells." In Thyroid Autoimmunity, 319–21. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-0945-1_45.

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5

Arnold, Bernd, Günther Schönrich, Iris Ferber, Judith Alferink, and Günter J. Hämmerling. "Tolerance induction in mature peripheral T cells." In Autoimmunity: Experimental Aspects, 1–9. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-78779-9_1.

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6

Shevach, Ethan M. "Integrins, γδ T Cells, and Autoimmunity." In Advances in Experimental Medicine and Biology, 49–55. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3396-2_7.

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7

Natvig, Jacob B., Kay B. Wilson, Alison Quayle, Sel Suleyman, Jens Kjeldsen-Kragh, Øystein Førre, Mouldy Sioud, and J. Donald Capra. "T cell receptor variable gene repertoire in rheumatoid synovial T cells responding to BCG." In Autoimmunity: Experimental Aspects, 191–96. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-78779-9_15.

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8

Kumar, Vipin, and Eli Sergarz. "The maintenance and reestablishment of self-tolerance: T cell receptor (TCR) peptide-specific regulatory T cells." In Autoimmunity: Experimental Aspects, 29–37. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-78779-9_3.

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9

Seddon, Benedict. "The Physiological Role of Regulatory T Cells in the Prevention of Autoimmunity: Generation, Specificity and Mode of Action." In Autoimmunity, 27–38. Dordrecht: Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-010-0981-2_3.

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10

Shevach, Ethan M., Rebecca S. McHugh, Angela M. Thornton, Ciriaco Piccirillo, Kannan Natarajan, and David H. Margulies. "Control of Autoimmunity by Regulatory T Cells." In Advances in Experimental Medicine and Biology, 21–32. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1243-1_3.

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Тези доповідей конференцій з теми "Immunometabolism, T cells, autoimmunity"

1

Rovere-Querini, Patrizia. "SP0103 T LYMPHOCYTES AND INNATE IMMUNE CELLS BALANCE MUSCLE REGENERATION AND AUTOIMMUNITY." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.8577.

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2

Gilmour, Cassandra, Seong-Keun (Steve) Yoo, Timothy Chan, and Lily Wang. "Abstract PR02: The co-expression of VISTA and TIGIT on cytotoxic T cells defines subpopulation with altered immunometabolism." In Abstracts: AACR Virtual Special Conference: Tumor Immunology and Immunotherapy; October 5-6, 2021. American Association for Cancer Research, 2022. http://dx.doi.org/10.1158/2326-6074.tumimm21-pr02.

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3

Hope, Jennifer L., Dennis C. Otero, Eun-ah Bae, Christopher J. Stairiker, Ashley B. Palete, Hannah A. Faso, Petrus de Jong, Garth Powis, and Linda M. Bradley. "Abstract PO014: PSGL-1 is an early T cell signaling regulator that drives immunometabolism and terminal differentiation in tumor-specific CD8 T cells." 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-po014.

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4

Alissafi, Themis, Aggelos Banos, Louis Boon, Tim Sparwasser, Dimitrios Vassilopoulos, Dimitrios Boumpas, Triantafyllos Chavakis, Kenneth Cadwell, and Panayotis Verginis. "03.16 Regulatory t cells restrain autophagy in dendritic cells to ameliorate autoimmunity in a ctla4 dependent fashion." In 37th European Workshop for Rheumatology Research 2–4 March 2017 Athens, Greece. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2016-211049.16.

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5

He, J., X. Sun, J. Li, R. Zhang, D. Yu, and Z. Li. "276 Low-dose il-2 circumvented mtor signallingsignaling in t cells in the treatment of sle." In LUPUS 2017 & ACA 2017, (12th International Congress on SLE &, 7th Asian Congress on Autoimmunity). Lupus Foundation of America, 2017. http://dx.doi.org/10.1136/lupus-2017-000215.276.

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6

Zhao, M., M. Li, and Q. Lu. "336 Defect of bdh2 contributes to dna hypomethylation in cd4+ t cells of systemic lupus erythematosus." In LUPUS 2017 & ACA 2017, (12th International Congress on SLE &, 7th Asian Congress on Autoimmunity). Lupus Foundation of America, 2017. http://dx.doi.org/10.1136/lupus-2017-000215.336.

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7

Nakayamada, S., S. Kubo, M. Yoshikawa, Y. Miyazaki, K. Sakata, K. Nakano, S. Iwata, I. Miyagawa, K. Saito, and Y. Tanaka. "52 The pathogenic relevance of t follicular helper cells-plasmablasts axis in patients with systemic lupus erythematosus." In LUPUS 2017 & ACA 2017, (12th International Congress on SLE &, 7th Asian Congress on Autoimmunity). Lupus Foundation of America, 2017. http://dx.doi.org/10.1136/lupus-2017-000215.52.

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8

Mo, W., S. Yin, H. Chen та X. Zhang. "74 Inflammatory vδ2 t cells chemotaxis to the joints and contribute to the pathogenesis of rheumatoid arthritis". У LUPUS 2017 & ACA 2017, (12th International Congress on SLE &, 7th Asian Congress on Autoimmunity). Lupus Foundation of America, 2017. http://dx.doi.org/10.1136/lupus-2017-000215.74.

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9

Orduno, N. Manjarrez, L. Menard, J. Carman, S. Suchard, F. Casano, D. Lee, S. Daouti, et al. "292 High frequency of circulating terminally differentiated cd8+ t cells characterise systemic lupus erythematosus patients with renal involvement." In LUPUS 2017 & ACA 2017, (12th International Congress on SLE &, 7th Asian Congress on Autoimmunity). Lupus Foundation of America, 2017. http://dx.doi.org/10.1136/lupus-2017-000215.292.

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10

Zhong, W., L. Zhao, Z. Jiang, and Y. Jiang. "57 A higher frequencies of t helper 22 cells in patients with new onset active systemic lupus erythematosus." In LUPUS 2017 & ACA 2017, (12th International Congress on SLE &, 7th Asian Congress on Autoimmunity). Lupus Foundation of America, 2017. http://dx.doi.org/10.1136/lupus-2017-000215.57.

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