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Libri sul tema "Regulatory T cell"

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Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 11 marzo 2023

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1

Ono, Masahiro, a cura di. Regulatory T-Cells. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-2647-4.

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2

Kassiotis, George, e Adrian Liston, a cura di. Regulatory T Cells. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61737-979-6.

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3

Taams, Leonie S., Marca H. M. Wauben e Arne N. Akbar, a cura di. Regulatory T Cells in Inflammation. Basel: Birkhäuser Basel, 2005. http://dx.doi.org/10.1007/b137037.

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4

Jiang, Shuiping, a cura di. Regulatory T Cells and Clinical Application. New York, NY: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-77909-6.

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5

Shuiping, Jiang, a cura di. Regulatory T cells and clinical application. New York: Springer, 2008.

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6

Regulatory T cells: Methods and protocols. [New York]: Humana Press, 2011.

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7

Zheng, Song-Guo, a cura di. T Regulatory Cells in Human Health and Diseases. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-15-6407-9.

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8

Compans, R. W., M. D. Cooper, T. Honjo, H. Koprowski, F. Melchers, M. B. A. Oldstone, S. Olsnes et al., a cura di. CD4+CD25+ Regulatory T Cells: Origin, Function and Therapeutic Potential. Berlin, Heidelberg: Springer Berlin Heidelberg, 2005. http://dx.doi.org/10.1007/3-540-27702-1.

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9

Na, Songqing, e Chandrasekar Venkataraman Iyer. Effector CD4+ T cells in health and disease 2007. Kerala, India: Transworld Research Network, 2007.

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10

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

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11

Carabin Is a Negative Regulator of Cd8+ T-cell-mediated Anti-tumor Immunity. [New York, N.Y.?]: [publisher not identified], 2022.

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12

L, Croxford J., e Yamamura T, a cura di. The immuno-regulatory role of natural killer T cells in inflammatory disease. Kerala: Research Signpost, 2005.

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13

I, Gabrilovich Dmitry, e Hurwitz Arthur A, a cura di. Tumor-induced immune suppression: Mechanisms and therapeutic reversal. New York, NY: Springer, 2008.

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14

Smith, Kendall A., a cura di. The Molecular Mechanisms of Regulatory T cell Immunosuppression. Frontiers Media SA, 2013. http://dx.doi.org/10.3389/978-2-88919-093-5.

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15

Kolodin, Dmitriy Pavlovich. Dynamics of Tissue-Resident Regulatory T Cell Populations. 2014.

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16

Wong, Jamie Evan. The life of the regulatory T cell repertoire. 2007.

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17

Alexander, Michael A. Functional and Translational Immunology of Regulatory T Cells (Tregs), the Anti-Tumor T Cell Response, and Cancer. Nova Science Publishers, Incorporated, 2014.

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18

Dominguez-Villar, Margarita, Lucy S. K. Walker e Silvia Piconese, a cura di. Control of Regulatory T cell Stability, Plasticity and Function in Health and Disease. Frontiers Media SA, 2021. http://dx.doi.org/10.3389/978-2-88966-570-9.

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19

Thomson, Christopher W. The role of FCRgamma in double negative T regulatory cell function and their expansion by lentivirally-transduced dendritic cells. 2006.

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20

Eljaafari, Assia, e Pierre Miossec. Cellular side of acquired immunity (T cells). Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0049.

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Abstract (sommario):

The adaptive T-cell response represents the most sophisticated component of the immune response. Foreign invaders are recognized first by cells of the innate immune system. This leads to a rapid and non-specific inflammatory response, followed by induction of the adaptive and specific immune response. Different adaptive responses can be promoted, depending on the predominant effector cells that are involved, which themselves depend on the microbial/antigen stimuli. As examples, Th1 cells contribute to cell-mediated immunity against intracellular pathogens, Th2 cells protect against parasites, and Th17 cells act against extracellular bacteria and fungi that are not cleared by Th1 and Th2 cells. Among the new subsets, Th22 cells protect against disruption of epithelial layers secondary to invading pathogens. Finally these effector subsets are regulated by regulatory T cells. These T helper subsets counteract each other to maintain the homeostasis of the immune system, but this balance can be easily disrupted, leading to chronic inflammation or autoimmune diseases. The challenge is to detect early changes in this balance, prior to its clinical expression. New molecular tools such as microarrays could be used to determine the predominant profile of the immune effector cells involved in a disease process. Such understanding should provide better therapeutic tools to counteract deregulated effector cells.

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21

Regulatory T cells. Copenhagen: Munksgaard, 2001.

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22

Lu, Ling, Bruce Blazar e Fadi Issa, a cura di. Regulatory T Cells. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88976-810-3.

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23

Regulatory T-Cells. Elsevier, 2011. http://dx.doi.org/10.1016/c2009-0-00167-6.

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24

Rudensky, Alexander, e Shimon Sakaguchi. Regulatory T-Cells. Elsevier Science & Technology Books, 2011.

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25

Regulatory T cells. Copenhagen: Munksgaard, 2001.

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26

Hayashi, Ren S. Regulatory T Cells. Nova Science Publishers, Incorporated, 2011.

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27

Regulatory T Cells [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.98075.

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28

Taams, Leonie S., Arne N. Akbar e Marca H. M. Wauben. Regulatory T Cells in Inflammation. Springer London, Limited, 2005.

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29

Leonie S. Taams,Arne N. Akbar,Marca H. M. Wauben. Regulatory T Cells in Inflammation. Springer, 2008.

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30

Cvetanovich, Gregory. Molecular regulatory circuitry of human regulatory T cells and Th17 cells. 2012.

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31

Regulatory Tcells. Academic Press, 2011.

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32

Tsai, Ching-Wei, Sanjeev Noel e Hamid Rabb. Pathophysiology of Acute Kidney Injury, Repair, and Regeneration. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0030.

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Abstract (sommario):

Acute kidney injury (AKI), regardless of its aetiology, can elicit persistent or permanent kidney tissue changes that are associated with progression to end-stage renal disease and a greater risk of chronic kidney disease (CKD). In other cases, AKI may result in complete repair and restoration of normal kidney function. The pathophysiological mechanisms of renal injury and repair include vascular, tubular, and inflammatory factors. The initial injury phase is characterized by rarefaction of peritubular vessels and engagement of the immune response via Toll-like receptor binding, activation of macrophages, dendritic cells, natural killer cells, and T and B lymphocytes. During the recovery phase, cell adhesion molecules as well as cytokines and chemokines may be instrumental by directing the migration, differentiation, and proliferation of renal epithelial cells; recent data also suggest a critical role of M2 macrophage and regulatory T cell in the recovery period. Other processes contributing to renal regeneration include renal stem cells and the expression of growth hormones and trophic factors. Subtle deviations in the normal repair process can lead to maladaptive fibrotic kidney disease. Further elucidation of these mechanisms will help discover new therapeutic interventions aimed at limiting the extent of AKI and halting its progression to CKD or ESRD.

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33

Kassiotis, George, e Adrian Liston. Regulatory T Cells: Methods and Protocols. Humana Press, 2016.

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34

Jiang, Shuiping. Regulatory T Cells and Clinical Application. Springer London, Limited, 2008.

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35

Ono, Masahiro. Regulatory T-Cells: Methods and Protocols. Springer, 2022.

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36

Jiang, Shuiping. Regulatory T Cells and Clinical Application. Springer, 2010.

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37

Liston, Adrian. Regulatory T Cells in Health and Disease. Elsevier Science & Technology Books, 2015.

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38

Liston, Adrian. Regulatory T Cells in Health and Disease. Elsevier Science & Technology, 2015.

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39

Regulatory T Cells in Health and Disease. Elsevier, 2015. http://dx.doi.org/10.1016/s1877-1173(15)x0008-1.

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40

Shvets, Anna. B7H4, a negative regulator of T cell immunity. 2006.

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41

van der Vlag, Johan, e Jo H. M. Berden. The patient with systemic lupus erythematosus. A cura di Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0161.

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Abstract (sommario):

Systemic lupus erythematosus (SLE) is a systemic autoimmune disease with various clinical manifestations. The hallmark of SLE is the presence of antibodies against nuclear constituents, such as double-stranded (ds)DNA, histones, and nucleosomes. Local deposition of antinuclear antibodies in complex with nuclear autoantigens induces serious inflammatory conditions that can affect several tissues and organs, including the kidney.The levels of antinucleosome and anti-dsDNA antibodies seem to correlate with glomerulonephritis and these autoantibodies can often be detected years before the patient is diagnosed with SLE. Apoptotic debris is present in the extracellular matrix and circulation of patients with SLE due to an aberrant process of apoptosis and/or insufficient clearance of apoptotic cells and apoptotic debris. The non-cleared apoptotic debris in patients with SLE may lead to activation of both the innate (myeloid and plasmacytoid dendritic cells) and adaptive (T and B cells) immune system. In addition to the activation by apoptotic debris and immune complexes, the immune system in SLE may be deregulated at the level of (a) presentation of self-peptides by antigen-presenting cells, (b) selection processes for both B and T cells, and (c) regulatory processes of B- and T-cell responses. Lupus nephritis may be classified in different classes based on histological findings in renal biopsies. The chromatin-containing immune complexes deposit in the capillary filter, most likely due to the interaction of chromatin with the polysaccharide heparan sulphate. A decreased renal expression of the endonuclease DNaseI further contributes to the glomerular persistence of chromatin and the development of glomerulonephritis.Current treatment of lupus nephritis is not specific and aims to reduce the inflammatory response with general immunosuppressive therapies. However, research has revealed novel potential therapeutic candidates at the level of dendritic cells, B cells, and T cells.

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42

Skuljec, Jelena, Christine Happle e Maria Grazia Roncarolo, a cura di. Therapeutic Potential of Gene-Modified Regulatory T Cells. Frontiers Media SA, 2021. http://dx.doi.org/10.3389/978-2-88971-847-4.

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43

Zheng, Song-Guo. T Regulatory Cells in Human Health and Diseases. Springer Singapore Pte. Limited, 2022.

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44

Zheng, Song-Guo. T Regulatory Cells in Human Health and Diseases. Springer, 2021.

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45

Goode, Jamie A., Gregory R. Bock e Novartis Foundation Symposium Staff. Generation and Effector Functions of Regulatory Lymphocytes. Wiley & Sons, Incorporated, John, 2008.

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46

(Editor), Leonie S. Taams, Arne N. Akbar (Editor) e Marca H.M. Wauben (Editor), a cura di. Regulatory T Cells in Inflammation (Progress in Inflammation Research). Birkhäuser Basel, 2005.

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47

Kyewski, B., e Elisabeth Suri-Payer. CD4+CD25+ Regulatory T Cells: Origin, Function and Therapeutic Potential. Springer London, Limited, 2006.

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48

Kyewski, B., e Elisabeth Suri-Payer. CD4+CD25+ Regulatory T Cells: Origin, Function and Therapeutic Potential. Springer, 2010.

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49

Miljkovic, Djordje, e Piotr Trzonkowski, a cura di. Tolerogenic Dendritic Cells and Regulatory T Cells as Therapeutics for Immune-Mediated Disorders. Frontiers Media SA, 2021. http://dx.doi.org/10.3389/978-2-88971-646-3.

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50

Elkord, Eyad, a cura di. Thymus-derived, peripherally-derived and in vitro-induced T regulatory cells. Frontiers Media SA, 2014. http://dx.doi.org/10.3389/978-2-88919-234-2.

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