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Journal articles on the topic 'Immunometabolism, T cells, autoimmunity'

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Author: Grafiati

Published: 11 March 2023

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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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Walter, Ulrich, and Pere Santamaria. "CD8+ T cells in autoimmunity." Current Opinion in Immunology 17, no. 6 (December 2005): 624–31. http://dx.doi.org/10.1016/j.coi.2005.09.014.

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12

Yin, Zhinan, and Joe Craft. "γδ T cells in autoimmunity." Springer Seminars in Immunopathology 22, no. 3 (September 2000): 311–20. http://dx.doi.org/10.1007/s002810000048.

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13

Choileain, Niamh Ni, and H. P. Redmond. "Regulatory T-Cells and Autoimmunity." Journal of Surgical Research 130, no. 1 (January 2006): 124–35. http://dx.doi.org/10.1016/j.jss.2005.07.033.

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14

Leavy, Olive. "Regulatory T cells in autoimmunity." Nature Reviews Immunology 7, no. 5 (May 2007): 322–23. http://dx.doi.org/10.1038/nri2078.

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15

Duarte, João H. "CAR-T cells tackle autoimmunity." Nature Biotechnology 40, no. 11 (November 2022): 1575. http://dx.doi.org/10.1038/s41587-022-01576-9.

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16

Mohammadnezhad, Leila, Mojtaba Shekarkar Azgomi, Marco Pio La Manna, Guido Sireci, Chiara Rizzo, Giusto Davide Badami, Bartolo Tamburini, Francesco Dieli, Giuliana Guggino, and Nadia Caccamo. "Metabolic Reprogramming of Innate Immune Cells as a Possible Source of New Therapeutic Approaches in Autoimmunity." Cells 11, no. 10 (May 17, 2022): 1663. http://dx.doi.org/10.3390/cells11101663.

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Immune cells undergo different metabolic pathways or immunometabolisms to interact with various antigens. Immunometabolism links immunological and metabolic processes and is critical for innate and adaptive immunity. Although metabolic reprogramming is necessary for cell differentiation and proliferation, it may mediate the imbalance of immune homeostasis, leading to the pathogenesis and development of some diseases, such as autoimmune diseases. Here, we discuss the effects of metabolic changes in autoimmune diseases, exerted by the leading actors of innate immunity, and their role in autoimmunity pathogenesis, suggesting many immunotherapeutic approaches.

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17

Monferrer, Ezequiel, Sabina Sanegre, Isaac Vieco-Martí, Amparo López-Carrasco, Fernando Fariñas, Antonio Villatoro, Sergio Abanades, et al. "Immunometabolism Modulation in Therapy." Biomedicines 9, no. 7 (July 9, 2021): 798. http://dx.doi.org/10.3390/biomedicines9070798.

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The study of cancer biology should be based around a comprehensive vision of the entire tumor ecosystem, considering the functional, bioenergetic and metabolic state of tumor cells and those of their microenvironment, and placing particular importance on immune system cells. Enhanced understanding of the molecular bases that give rise to alterations of pathways related to tumor development can open up new therapeutic intervention opportunities, such as metabolic regulation applied to immunotherapy. This review outlines the role of various oncometabolites and immunometabolites, such as TCA intermediates, in shaping pro/anti-inflammatory activity of immune cells such as MDSCs, T lymphocytes, TAMs and DCs in cancer. We also discuss the extraordinary plasticity of the immune response and its implication in immunotherapy efficacy, and highlight different therapeutic intervention possibilities based on controlling the balanced systems of specific metabolites with antagonistic functions.

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18

Fu, Sicheng, Shasha Zhu, Chenxi Tian, Shiyu Bai, Jiqian Zhang, Chonglun Zhan, Di Xie, et al. "Immunometabolism regulates TCR recycling and iNKT cell functions." Science Signaling 12, no. 570 (February 26, 2019): eaau1788. http://dx.doi.org/10.1126/scisignal.aau1788.

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Invariant natural killer T (iNKT) cells are innate-like T lymphocytes that express an invariant T cell receptor (TCR), which recognizes glycolipid antigens presented on CD1d molecules. These cells are phenotypically and functionally distinct from conventional T cells. When we characterized the metabolic activity of iNKT cells, consistent with their activated phenotype, we found that they had much less mitochondrial respiratory capacity but increased glycolytic activity in comparison to naïve conventional CD4+ T cells. After TCR engagement, iNKT cells further increased aerobic glycolysis, which was important for the expression of interferon-γ (IFN-γ). Glycolytic metabolism promoted the translocation of hexokinase-II to mitochondria and the activation of mammalian target of rapamycin complex 2 (mTORC2). Inhibiting glycolysis reduced the activity of Akt and PKCθ, which inhibited TCR recycling and accumulation within the immune synapse. Diminished TCR accumulation in the immune synapse reduced the activation of proximal and distal TCR signaling pathways and IFN-γ production in activated iNKT cells. Our studies demonstrate that glycolytic metabolism augments TCR signaling duration and IFN-γ production in iNKT cells by increasing TCR recycling.

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19

Zhu, Yangyang, Le Zou, and Yun-Cai Liu. "T follicular helper cells, T follicular regulatory cells and autoimmunity." International Immunology 28, no. 4 (December 29, 2015): 173–79. http://dx.doi.org/10.1093/intimm/dxv079.

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20

McGuire, Peter J. "Chemical individuality in T cells: A Garrodian view of immunometabolism." Immunological Reviews 295, no. 1 (March 31, 2020): 82–100. http://dx.doi.org/10.1111/imr.12854.

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21

Barra, Nicole G., Fernando F. Anhê, and Jonathan D. Schertzer. "Immunometabolism Sentinels: Gut Surface T-Cells Regulate GLP-1 Availability." Endocrinology 160, no. 5 (April 8, 2019): 1177–78. http://dx.doi.org/10.1210/en.2019-00215.

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22

Lourenço, Elaine V., and Antonio La Cava. "Natural regulatory T cells in autoimmunity." Autoimmunity 44, no. 1 (November 23, 2010): 33–42. http://dx.doi.org/10.3109/08916931003782155.

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23

Mueller, K. L. "Engineering T cells to treat autoimmunity." Science 353, no. 6295 (July 7, 2016): 133–34. http://dx.doi.org/10.1126/science.353.6295.133-e.

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24

Kasper, Isaac R., Sokratis A. Apostolidis, Amir Sharabi, and George C. Tsokos. "Empowering Regulatory T Cells in Autoimmunity." Trends in Molecular Medicine 22, no. 9 (September 2016): 784–97. http://dx.doi.org/10.1016/j.molmed.2016.07.003.

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25

Costantino, Cristina M., Clare M. Baecher-Allan, and David A. Hafler. "Human regulatory T cells and autoimmunity." European Journal of Immunology 38, no. 4 (April 2008): 921–24. http://dx.doi.org/10.1002/eji.200738104.

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26

Shoenfeld, Yehuda. "Autoimmunity, T cells and immune regulation." Journal of Neuroimmunology 35 (January 1991): 2. http://dx.doi.org/10.1016/0165-5728(91)90831-q.

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27

Rolot, Marion, and Timothy E. O’Sullivan. "Retraction: Rolot, M.; O’Sullivan, T.E. Living with Yourself: Innate Lymphoid Cell Immunometabolism. Cells 2020, 9, 334." Cells 11, no. 16 (August 17, 2022): 2555. http://dx.doi.org/10.3390/cells11162555.

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28

Yin, Yiming, Todd Metzger, and Samantha Bailey-Bucktrout. "Tumor infiltrating T cells have abnormal lipid metabolism that can be modulated by PD-L1 blockade." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 144.21. http://dx.doi.org/10.4049/jimmunol.196.supp.144.21.

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Abstract T cell activation and function are tightly regulated by nutrient availability and cellular metabolism. The solid tumor environment has several attributes that affect the metabolism of tumor infiltrating T cells (TILs). For example, tumor cells compete with T cells for glucose and thereby limit T cell effector function. Moreover, highly hypoxic conditions that are found in the tumor environment impair the oxidative metabolism of T cells. Checkpoint inhibitory and co-stimulatory pathways have been shown to regulate T cell metabolism, indicating that cancer immunotherapies may modulate T cell function via metabolic processes. Here we show that tumor infiltrating T cells have abnormally high fatty acid uptake and lipid content, which is associated with increased expression of CD36, a fatty acid transporter. The abnormal metabolism is associated with the expression of exhaustion markers programmed death-1 (PD-1) and T-cell immunoglobulin and mucin-domain containing-3 (TIM3) and is due to the cancer microenvironment rather than antigen exposure. Blocking PD-1 signaling in vivo significantly reduced tumor progression and normalized lipid metabolism. In summary, immunometabolism including lipid metabolism can serve as biomarkers of T cell anti-tumor efficacy. Targeting immunometabolism represents a promising venue in cancer immunotherapy.

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29

Han, Feifei, Gonghua Li, Shaoxing Dai, and Jingfei Huang. "Genome-wide metabolic model to improve understanding of CD4+ T cell metabolism, immunometabolism and application in drug design." Molecular BioSystems 12, no. 2 (2016): 431–43. http://dx.doi.org/10.1039/c5mb00480b.

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30

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. "Immunometabolism regulation by PSGL-1 signaling in tumor-specific CD8 T cells." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 240.1. http://dx.doi.org/10.4049/jimmunol.204.supp.240.1.

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Abstract We previously identified that the adhesion molecule P-selectin glycoprotein ligand-1 (PSGL-1) regulates T cell function and exhaustion in response to chronic viral infection and tumors. Subsequent studies have focused on investigating the role of PSGL-1 signaling in T cell responses, with an emphasis on understanding the mechanisms by which PSGL-1 regulates T cell exhaustion. Single-cell RNA-sequencing of tumor infiltrating PSGL-1−/− CD8+ T cells identified the upregulation and differential modulation of several genes associated with T cell metabolism and enhanced intratumoral responses, including Mtor, Hif1a, and Mki67 in Gzmb/Ifng double-positive cells from tumors and Tcf7 in both tumor draining and non-draining inguinal lymph nodes. These data suggest an important role for PSGL-1 signaling in the development and maintenance of effective anti-tumor T cell responses to melanoma. Using the Seahorse glycolysis stress test, we identified that both CD4+ and CD8+ PSGL-1−/− T cells demonstrate increased glycolysis after 72 hours of in vitro activation compared to wild-type T cells. In situ activation of PSGL-1−/− CD8+ T cells demonstrated that PSGL-1−/− CD8+ T cells have increased glycolysis and increased glycolytic capacity at both sub-optimal and optimal levels of α-CD3 stimulation, and 2-NBDG glucose uptake assays confirmed increased glucose uptake by PSGL-1−/− CD8+ T cells within two hours of stimulation. Importantly, this increased glycolytic phenotype does not come at the cost of CD8+ T cell stemness, as determined by TCF-1 staining. Taken together, these data show that PSGL-1 signaling has an intrinsic and immediate role in the development of T cell responses and their metabolic profile in response to melanoma tumors.

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31

Shyer, Justin A., Richard A. Flavell, and Will Bailis. "Metabolic signaling in T cells." Cell Research 30, no. 8 (July 24, 2020): 649–59. http://dx.doi.org/10.1038/s41422-020-0379-5.

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Abstract The maintenance of organismal homeostasis requires partitioning and transport of biochemical molecules between organ systems, their composite cells, and subcellular organelles. Although transcriptional programming undeniably defines the functional state of cells and tissues, underlying biochemical networks are intricately intertwined with transcriptional, translational, and post-translational regulation. Studies of the metabolic regulation of immunity have elegantly illustrated this phenomenon. The cells of the immune system interface with a diverse set of environmental conditions. Circulating immune cells perfuse peripheral organs in the blood and lymph, patrolling for pathogen invasion. Resident immune cells remain in tissues and play more newly appreciated roles in tissue homeostasis and immunity. Each of these cell populations interacts with unique and dynamic tissue environments, which vary greatly in biochemical composition. Furthermore, the effector response of immune cells to a diverse set of activating cues requires unique cellular adaptations to supply the requisite biochemical landscape. In this review, we examine the role of spatial partitioning of metabolic processes in immune function. We focus on studies of lymphocyte metabolism, with reference to the greater immunometabolism literature when appropriate to illustrate this concept.

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32

Veldhoen, Marc, and Benedict Seddon. "Empowering T helper 17 cells in autoimmunity." Nature Medicine 16, no. 2 (February 2010): 166–68. http://dx.doi.org/10.1038/nm0210-166.

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33

Kitz, Alexandra, Emily Singer, and David Hafler. "Regulatory T Cells: From Discovery to Autoimmunity." Cold Spring Harbor Perspectives in Medicine 8, no. 12 (January 8, 2018): a029041. http://dx.doi.org/10.1101/cshperspect.a029041.

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34

Mellanby, Richard J., David C. Thomas, and Jonathan Lamb. "Role of regulatory T-cells in autoimmunity." Clinical Science 116, no. 8 (March 16, 2009): 639–49. http://dx.doi.org/10.1042/cs20080200.

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There has been considerable historical interest in the concept of a specialist T-cell subset which suppresses over-zealous or inappropriate T-cell responses. However, it was not until the discovery that CD4+CD25+ T-cells had suppressive capabilities both in vitro and in vivo that this concept regained credibility and developed into one of the most active research areas in immunology today. The notion that in healthy individuals there is a subset of Treg-cells (regulatory T-cells) involved in ‘policing’ the immune system has led to the intensive exploration of the role of this subset in disease resulting in a number of studies concluding that a quantitative or qualitative decline in Treg-cells is an important part of the breakdown in self-tolerance leading to the development of autoimmune diseases. Although Treg-cells have subsequently been widely postulated to represent a potential immunotherapy option for patients with autoimmune disease, several studies of autoimmune disorders have demonstrated high numbers of Treg-cells in inflamed tissue. The present review highlights the need to consider a range of other factors which may be impairing Treg-cell function when considering the mechanisms involved in the breakdown of self-tolerance rather than focussing on intrinsic Treg-cell factors.

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35

Rowland-Jones, Sarah, and Tao Dong. "Dying T cells trigger autoimmunity in HIV." Nature Medicine 13, no. 12 (December 2007): 1413–15. http://dx.doi.org/10.1038/nm1207-1413.

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36

Ueno, Hideki. "T follicular helper cells in human autoimmunity." Current Opinion in Immunology 43 (December 2016): 24–31. http://dx.doi.org/10.1016/j.coi.2016.08.003.

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37

Mueller, K. L. "Early T cells keep autoimmunity at bay." Science 348, no. 6234 (April 30, 2015): 536. http://dx.doi.org/10.1126/science.348.6234.536-p.

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38

STASTNY, PETER, LINDA K. MYERS, GABRIEL NUÑEZ, MARIE L. MARIE L, J. DONALD CAPRA, and EDWARD J. BALL. "Molecular Genetics and T Cells in Autoimmunity." Annals of the New York Academy of Sciences 475, no. 1 Autoimmunity (July 1986): 12–23. http://dx.doi.org/10.1111/j.1749-6632.1986.tb20852.x.

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39

Pellegrini, F. P., M. Marinoni, V. Frangione, A. Tedeschi, V. Gandini, F. Ciglia, L. Mortara, R. S. Accolla, and L. Nespoli. "Down syndrome, autoimmunity and T regulatory cells." Clinical & Experimental Immunology 169, no. 3 (August 2, 2012): 238–43. http://dx.doi.org/10.1111/j.1365-2249.2012.04610.x.

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40

Flemming, Alexandra. "CAR-T cells take aim at autoimmunity." Nature Reviews Drug Discovery 15, no. 9 (August 30, 2016): 603. http://dx.doi.org/10.1038/nrd.2016.180.

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41

von Herrath, Matthias G., and Leonard C. Harrison. "Antigen-induced regulatory T cells in autoimmunity." Nature Reviews Immunology 3, no. 3 (March 2003): 223–32. http://dx.doi.org/10.1038/nri1029.

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42

Kono, Michihito, Nobuya Yoshida, and George C. Tsokos. "Metabolic control of T cells in autoimmunity." Current Opinion in Rheumatology 32, no. 2 (March 2020): 192–99. http://dx.doi.org/10.1097/bor.0000000000000685.

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43

Hou, Lifei, Tian Wang, and Jiaren Sun. "γδ T cells in infection and autoimmunity." International Immunopharmacology 28, no. 2 (October 2015): 887–91. http://dx.doi.org/10.1016/j.intimp.2015.03.038.

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44

Kouame, Elaine, Pamela Brigleb, Kishan Sangani, Terence S. Dermody, and Bana Jabri. "The miseducation of T cells in autoimmunity." Journal of Immunology 208, no. 1_Supplement (May 1, 2022): 114.05. http://dx.doi.org/10.4049/jimmunol.208.supp.114.05.

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Abstract Celiac disease (CeD) is an immune-mediated enteropathy characterized by an inflammatory T-helper type 1 (Th1) immune response against dietary gluten. Although 40% of individuals in the U.S. have the genetic factors required for the development of CeD, less than 1% will be diagnosed with CeD. This suggests that additional environmental factors are necessary for the development of CeD. Our previous work demonstrates that viral infections can disrupt tolerance to oral antigens, leading to immune activation as seen in CeD. However, the mechanisms by which viral infections trigger inflammatory responses to dietary antigen remains unknown. Here we show that upon infection with reovirus, a subset of migratory dendritic cells, cDC1, sense and uptake virally infected and necroptotic intestinal epithelial cells and secrete type I interferon (IFN), resulting in a dietary antigen specific Th1 immune response. Our results identify a novel mechanism by which certain viruses can trigger inflammatory immune responses to dietary antigen. We also demonstrate that only a subset of enteric viruses can disrupt homeostatic response to dietary antigens. Only those that both induce type I IFN, and cause necroptosis will result in such pathology. This data identifies specific viral targets for clinical intervention via vaccine that could potentially reduce the incidence of CeD and other dietary-triggered immune enteropathies. More generally, knowledge from our work enhance our understanding of how viral-host interactions drive autoimmune disorders at the mucosal interface. Supported by grant from NIH (RO1 5R01DK098435-06)

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45

Mougiakakos, Dimitrios. "CAR-T cells: from cancer to autoimmunity." Cell and Gene Therapy Insights 08, no. 10 (November 10, 2022): 1143–50. http://dx.doi.org/10.18609/cgti.2022.171.

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Posnett, D. N., A. Gottlieb, J. B. Bussel, S. M. Friedman, N. Chiorazzi, Y. Li, P. Szabo, N. R. Farid, and M. A. Robinson. "T cell antigen receptors in autoimmunity." Journal of Immunology 141, no. 6 (September 15, 1988): 1963–69. http://dx.doi.org/10.4049/jimmunol.141.6.1963.

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Abstract Three mAb to variable region determinants of the alpha/beta-chain TCR were used to detect discrete populations of peripheral blood T cells. T cells sharing a TCR determinant defined by such an antibody presumably use the same or similar TCR V or J genes for their alpha- or beta-chains. Thus analysis with these mAb provides a tool to investigate TCR gene usage and expression. Since autoantigen specific T cells may play an important role in initiating autoimmune diseases, TCR were analyzed in different autoimmune diseases and control groups including rheumatoid arthritis, Graves disease, idiopathic thrombocytopenic purpura, psoriasis, SLE, insulin-dependent diabetes mellitus, and in nonautoimmune control diseases and normals. Purified T cells were stained by indirect immunofluorescence with three mAb to TCR variable regions: mAb S511 stains 1.8 +/- 0.9% (mean +/- 2 SD), mAb C37 stains 3.4 +/- 1.5% and mAb OT145 stains from 0 to 6% of T cells from normal donors. Several individuals were identified with expanded subsets of positive T cells. One patient with adult ITP followed during a 12-mo period consistently had elevated percentages of T cells staining with the mAb OT145 (15.9 to 24.5%). These cells were found to be exclusively CD8+. By Southern blotting DNA prepared from these OT145+, CD8+ cells, but not DNA from the patient's OT145- T cells, revealed a clonal rearrangement using a beta-chain C region probe. Thus this patient had a monoclonal expansion of CD8+, OT145+ cells. Hyperexpression of a TCR variable region, as defined by the available mAb, could not be associated with any of the diseases studied. Examination of T cells at the site of autoimmunity, such as T cells from rheumatoid arthritis synovial fluid, revealed normal percentages of cells staining with these mAb. Immunoperoxidase staining of psoriatic lesional skin showed no striking enrichment of T cells bearing one or the other TCR type.

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Poznanski, Sophie M., Nicole G. Barra, Ali A. Ashkar, and Jonathan D. Schertzer. "Immunometabolism of T cells and NK cells: metabolic control of effector and regulatory function." Inflammation Research 67, no. 10 (July 31, 2018): 813–28. http://dx.doi.org/10.1007/s00011-018-1174-3.

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Elliott, J. I., and D. M. Altmann. "Dual T cell receptor alpha chain T cells in autoimmunity." Journal of Experimental Medicine 182, no. 4 (October 1, 1995): 953–59. http://dx.doi.org/10.1084/jem.182.4.953.

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Allelic exclusion at the T cell receptor alpha locus TCR-alpha is incomplete, as demonstrated by the presence of a number of T lymphocyte clones carrying two expressed alpha chain products. Such dual alpha chain T cells have been proposed to play a role in autoimmunity, for example, because of a second TCR-alpha beta pair having bypassed negative selection by virtue of low expression. We examined this hypothesis by generating mice of various autoimmunity-prone strains carrying a hemizygous targeted disruption of the TCR-alpha locus, therefore unable to produce dual alpha chain T cells. Normal mice have a low but significant proportion of T cells expressing two cell-surface TCR-alpha chains that could be enumerated by comparison to TCR-alpha hemizygotes, which have none. Susceptibility to various autoimmune diseases was analyzed in TCR-alpha hemizygotes that had been backcrossed to disease-prone strains for several generations. The incidence of experimental allergic encephalomyelitis and of lupus is not affected by the absence of dual TCR-alpha cells. In contrast, nonobese diabetic (NOD) TCR alpha hemizygotes are significantly protected from cyclophosphamide-accelerated insulitis and diabetes. Thus, dual alpha T cells may play an important role in some but not all autoimmune diseases. Furthermore, since protected and susceptible NOD mice both show strong spontaneous responses to glutamic acid decarboxylase, responses to this antigen, if necessary for diabetetogenesis, are not sufficient.

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Luu, Maik, and Alexander Visekruna. "Short‐chain fatty acids: Bacterial messengers modulating the immunometabolism of T cells." European Journal of Immunology 49, no. 6 (May 17, 2019): 842–48. http://dx.doi.org/10.1002/eji.201848009.

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Alba, Gonzalo, Hala Dakhaoui, Consuelo Santa-Maria, Francisca Palomares, Marta Cejudo-Guillen, Isabel Geniz, Francisco Sobrino, Sergio Montserrat-de la Paz, and Soledad Lopez-Enriquez. "Nutraceuticals as Potential Therapeutic Modulators in Immunometabolism." Nutrients 15, no. 2 (January 13, 2023): 411. http://dx.doi.org/10.3390/nu15020411.

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Nutraceuticals act as cellular and functional modulators, contributing to the homeostasis of physiological processes. In an inflammatory microenvironment, these functional foods can interact with the immune system by modulating or balancing the exacerbated proinflammatory response. In this process, immune cells, such as antigen-presenting cells (APCs), identify danger signals and, after interacting with T lymphocytes, induce a specific effector response. Moreover, this conditions their change of state with phenotypical and functional modifications from the resting state to the activated and effector state, supposing an increase in their energy requirements that affect their intracellular metabolism, with each immune cell showing a unique metabolic signature. Thus, nutraceuticals, such as polyphenols, vitamins, fatty acids, and sulforaphane, represent an active option to use therapeutically for health or the prevention of different pathologies, including obesity, metabolic syndrome, and diabetes. To regulate the inflammation associated with these pathologies, intervention in metabolic pathways through the modulation of metabolic energy with nutraceuticals is an attractive strategy that allows inducing important changes in cellular properties. Thus, we provide an overview of the link between metabolism, immune function, and nutraceuticals in chronic inflammatory processes associated with obesity and diabetes, paying particular attention to nutritional effects on APC and T cell immunometabolism, as well as the mechanisms required in the change in energetic pathways involved after their activation.

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