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Books on the topic 'T cells. Natural immunity'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

A, Berzofsky Jay, and SpringerLink (Online service), eds. Natural Killer T cells: Balancing the Regulation of Tumor Immunity. New York, NY: Springer Science+Business Media, LLC, 2012.

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Guide to signal pathways in immune cells. New York: Springer Verlag, 2009.

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3

Wardle, E. N. Guide to signal pathways in immune cells. New York: Springer Verlag, 2009.

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4

Terabe, Masaki, and Jay A. Berzofsky, eds. Natural Killer T cells. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-0613-6.

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

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6

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

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7

Liu, Chaohong, ed. Invariant Natural Killer T-Cells. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1775-5.

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8

W, Ades Edwin, and Lopez Carlos 1942-, eds. Natural killer cells and host defense. Basel: Karger, 1989.

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9

Lane, I. William. Immune power. Garden City Park, NY: Avery Pub. Group, 1999.

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10

1951-, Schmidt Reinhold E., ed. Natural Killer cells: Biology and clinical application. Basel: Karger, 1990.

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11

service), SpringerLink (Online, ed. Innate and Adaptive Immunity in the Tumor Microenvironment. Dordrecht: Springer Science + Business Media, LLC, 2008.

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12

service), SpringerLink (Online, ed. Natural Killer Cells: At the Forefront of Modern Immunology. Berlin, Heidelberg: Springer-Verlag Berlin Heidelberg, 2010.

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13

John, Stewart. The primordial VRM system and the evolution of vertebrate immunity. Austin: R.G. Landes, 1994.

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14

Liu, Yang. The costimulatory pathway for T cell response. Austin: R.G. Landes, 1994.

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15

Lefkovits, Ivan. Limiting dilution analysis of cells of the immune system. 2nd ed. Oxford [England]: Oxford University Press, 1999.

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16

Handbook of ELISPOT: Methods and protocols. 2nd ed. New York: Humana Press, 2012.

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17

Carlos, Rodríguez-Gallego, and Arnaiz-Villena Antonio, eds. Human T-lymphocyte activation deficiencies. Austin, TX: R.G. Landes, 1994.

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18

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

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19

Gordin, Kaplan J., Green Doug R, and Bleackley R. Chris, eds. Cellular basis of immune modulation: Proceedings of the 19th International Leukocyte Culture Conference held at Banff Springs Hotel, Banff, Alberta, May 8-12, 1988. New York: A.R. Liss, 1988.

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20

Shah, Prakash Dhirajlal. Natural killer cells and accessory cells in T cell immunity. 1986.

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21

Berzofsky, Jay A., and Masaki Terabe. Natural Killer T cells: Balancing the Regulation of Tumor Immunity. Humana, 2013.

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22

Berzofsky, Jay A., and Masaki Terabe. Natural Killer T cells: Balancing the Regulation of Tumor Immunity. Springer, 2011.

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23

Rabinovich, Brian A. Innate regulation of adaptive immunity: Natural killer cell recognition of stressed and activated T cells. 2003.

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24

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

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25

(Editor), B. Pulendran, and R. Ahmed (Editor), eds. From Innate Immunity to Immunological Memory (Current Topics in Microbiology and Immunology). Springer, 2006.

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26

Immunity, Society for Natural. Nk Cells & Natural Immunity. S. Karger AG (Switzerland), 1995.

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27

Bent, Rolstad, ed. Natural immunity to normal hemopoietic cells. Boca Raton: CRC Press, 1994.

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28

Eljaafari, Assia, and 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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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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29

Bending, David, Kiran Nistala, and Lucy R. Wedderburn. Pathogenesis of juvenile idiopathic arthritis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0060.

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Although the term juvenile idiopathic arthritis (JIA) encompasses a heterogeneous group of diseases, they all share a common pathological hallmark: inflammation of the synovium. Highly activated T cells, monocytes, and neutrophils are attracted to the joint and secrete mediators that not only perpetuate inflammation but also may attenuate immune regulation. In the oligoarticular and polyarticular forms of JIA, which are thought to be autoimmune conditions, dysregulated adaptive immunity is a likely factor in disease pathogenesis; the nature of the interactions between T effector (Teff) cells and T regulatory cells (Treg) is probably a key factor in controlling disease progression. Factors that affect the frequency and function of Tregs and/or the sensitivity of Teffs to mechanisms of immune suppression will therefore impact on the disease course. In the systemic form of JIA, however, dysregulation of innate immune pathways appears more central to disease pathogenesis resulting in augmented levels of interleukins IL-1β‎, IL-6, and IL-18. In the end, a final, common pathological pathway in JIA is the activation of monocytes and neutrophils, which are the principal mediators of joint inflammation and damage. This is supported by the fact that the therapies that have targeted innate cytokine pathways have shown greater success in the treatment of JIA.

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30

Fousteri, Georgia, Shahram Salek-Ardakani, and Maria Pia Cicalese, eds. Follicular Helper T Cells in Immunity and Autoimmunity. Frontiers Media SA, 2020. http://dx.doi.org/10.3389/978-2-88963-847-5.

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31

E, Lewis Claire, and McGee J. O'D, eds. Natural Killer Cell: Natural Immune System. I.R.L. P., 1992.

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32

Haeryfar, S. M. Mansour, and Thierry Mallevaey, eds. CD1- and MR1-restricted T Cells in Antimicrobial Immunity. Frontiers Media SA, 2016. http://dx.doi.org/10.3389/978-2-88919-750-7.

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33

(Editor), Claire E. Lewis, and James O'D McGee (Editor), eds. The Natural Killer Cell: The Natural Immune System. Oxford University Press, USA, 1992.

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34

(Editor), Claire E. Lewis, and James O'D McGee (Editor), eds. The Natural Killer Cell: The Natural Immune System. Oxford University Press, USA, 1992.

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35

1936-, Lotzová Eva, and Herberman Ronald B. 1940-, eds. Immunobiology of natural killer cells. Boca Raton, Fla: CRC Press, 1986.

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36

E, Lewis Claire, and McGee J. O'D, eds. The Natural killer cell. Oxford: IRL Press at Oxford University Press, 1992.

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37

Current Topics in Innate Immunity. Springer, 2007.

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38

D, Lambris J., and International Conference on Innate Immunity (4th : Corfu, Greece : 2006), eds. Current topics in innate immunity. Berlin: Springer, 2007.

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39

Baldridge, Jory R. T cells which mediate protective immunity to Listeria Monocytogenes are H-2K restricted and distinct from the T cells mediating DTH. 1989.

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40

Lotzova, Eva, and Ronald B. Herberman. Immunobiology of Natural Killer Cells: Volume 2. Taylor & Francis Group, 2019.

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41

Lotzova, Eva, and Ronald B. Herberman. Immunobiology of Natural Killer Cells: Volume 2. Taylor & Francis Group, 2019.

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42

Lotzova, Eva, and Ronald B. Herberman. Immunobiology of Natural Killer Cells: Volume 2. Taylor & Francis Group, 2019.

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43

Lotzova, Eva, and Ronald B. Herberman. Immunobiology of Natural Killer Cells: Volume 2. Taylor & Francis Group, 2019.

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44

V, Fournier Nathan, ed. Natural killer T-cells: Roles, interactions, and interventions. New York: Nova Science Publishers, 2008.

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45

T, Vella Anthony, ed. Towards an understanding of initiating T cell immunity 2006. Trivandrum, Kerala, India: Research Signpost, 2006.

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46

1933-, Cooper Max D., and Koprowski Hilary, eds. The Interface between innate and acquired immunity. Berlin: Springer, 2002.

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47

(Editor), M. D. Cooper, and H. Koprowski (Editor), eds. The Interface Between Innate and Acquired Immunity (Current Topics in Microbiology and Immunology). Springer, 2002.

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48

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

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49

Iwabuchi, Kazuya, and Luc Van Kaer, eds. Role of CD1- and MR1-restricted T cells in Immunity and Disease. Frontiers Media SA, 2019. http://dx.doi.org/10.3389/978-2-88963-122-3.

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50

Dörner, Thomas, and Peter E. Lipsky. Cellular side of acquired immunity (B cells). Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0050.

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B cells have gained interest in rheumatoid arthritis (RA) beyond being the precursors of antibody-producing plasma cells since they are also a broader component of the adaptive immune system. They are capable of functioning as antigen-presenting cells for T-cell activation and can produce an array of cytokines. Disturbances of peripheral B-cell homeostasis together with the formation of ectopic lymphoid neogenesis within the inflamed synovium appears to be a characteristic of patients with RA. Enhanced generation of memory B cells and autoreactive plasma cells producing IgM-RF and ACPA-IgG antibodies together with formation of immune complexes contribute to the maintenance of RA, whereas treatment with B-cell-directed anti-CD20 therapy provides clinical benefit.

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