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Relevant bibliographies by topics / Immunometabolism, T cells, autoimmunity / Books

Books on the topic 'Immunometabolism, T cells, autoimmunity'

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Author: Grafiati

Published: 11 March 2023

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1

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

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2

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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5

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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9

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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11

Symposium in Immunology (1st 1991?). Symposium in Immunology I, Symposium in Immunology II. Berlin: Springer-Verlag, 1993.

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12

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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13

T-cell autoimmunity and multiple sclerosis. Austin: R.G. Landes, 1999.

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14

Adorini. Immunointervention in Autoimmunity. Springer, 1998.

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15

Perl, Andras. Autoimmunity: Methods and Protocols. Humana Press, 2016.

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16

Londei, Marco. T-Cell Autoimmunity and Multiple Sclerosis (Neuroscience Intelligence Unit 5) (Neuroscience Intelligence Unit). Landes Bioscience, 1999.

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17

Catalfamo, Marta, Sara Ferrando-Martinez, and Eva Reali, eds. The Interplay Between Immune Activation and Cardiovascular Disease During Infection, Autoimmunity and Aging: The Role of T Cells. Frontiers Media SA, 2021. http://dx.doi.org/10.3389/978-2-88971-232-8.

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18

(Editor), Domencio Gambi, Allesandra Lugaresi (Editor), and Paolo A. Muraro (Editor), eds. Advances in the Immunopathogenesis of Multiple Sclerosis. Springer, 1999.

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19

(Editor), Andrzej Mackiewicz, Maciej Kurpisz (Editor), and Jan Zeromski (Editor), eds. Progress in Basic and Clinical Immunology (Advances in Experimental Medicine and Biology). Springer, 2001.

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20

Mackiewicz, Andrzej. Progress in Basic and Clinical Immunology. Springer, 2012.

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21

Kurpisz, Maciej, Jan Zeromski, and Andrzej Mackiewicz. Progress in Basic and Clinical Immunology. Springer London, Limited, 2012.

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22

Foundation, Novartis. Generation and Effector Functions of Regulatory Lymphocytes (Novartis Foundation Symposia). Wiley, 2003.

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23

Progress in basic and clinical immunology. New York: Kluwer Academic/Plenum Publishers, 2001.

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24

Ahmed, Rafi, and Bali Pulendran. From Innate Immunity to Immunological Memory. Springer Berlin / Heidelberg, 2010.

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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

Piccio, Laura, and Anne H. Cross. Immunology of Multiple Sclerosis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199341016.003.0004.

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Multiple sclerosis (MS) is considered to be an autoimmune disease of the central nervous system that targets myelin but affects both white matter and gray matter. Multiple sclerosis is thought to be mediated by cells of the adaptive and innate immune systems. CD4+ T lymphocytes of the Th1 and Th17 subtypes are believed to be critical for the initiation of multiple sclerosis. Treatment with monoclonal antibodies that deplete B lymphocytes has proven that B cells are critical to relapse development in multiple sclerosis. While immunopathophysiology is clearly important in MS, whether multiple sclerosis is truly an autoimmune disorder and the target or targets of the autoimmunity remain unknown.

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27

Cerhan, James R., Claire M. Vajdic, and John J. Spinelli. The Non-Hodgkin Lymphomas. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0040.

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The non-Hodgkin lymphomas (NHL) are a heterogeneous group of over forty lymphoid neoplasms that have undergone a major redefinition over the last twenty-five years, in part due to advances in immunology and genetics as well as implementation of the WHO classification system. NHLs are considered clonal tumors of B-cells, T-cells, or natural killer (NK) cells arrested at various stages of differentiation, regardless of whether they present in the blood (lymphoid leukemia) or lymphoid tissues (lymphoma). In the United States, the age-standardized NHL incidence rate (per 100,000) doubled from 1973 (10.2) to 2004 (21.4) and then stabilized, while five-year relative survival rates improved from 42% in 1973 to 70% in 2004. Established risk factors for NHL or specific NHL subtypes include infectious agents (HTLV-1, HIV, EBV, HHV8, HCV, H. pylori), immune dysregulation (primary immunodeficiency, transplantation, autoimmunity, and immunosuppressive drugs), family history of lymphoma, and common genetic variants identified by genome-wide association studies.

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28

Voll, Reinhard E., and Barbara M. Bröker. Innate vs acquired immunity. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0048.

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The innate and the adaptive immune system efficiently cooperate to protect us from infections. The ancient innate immune system, dating back to the first multicellular organisms, utilizes phagocytic cells, soluble antimicrobial peptides, and the complement system for an immediate line of defence against pathogens. Using a limited number of germline-encoded pattern recognition receptors including the Toll-like, RIG-1-like, and NOD-like receptors, the innate immune system recognizes so-called pathogen-associated molecular patterns (PAMPs). PAMPs are specific for groups of related microorganisms and represent highly conserved, mostly non-protein molecules essential for the pathogens' life cycles. Hence, escape mutants strongly reduce the pathogen's fitness. An important task of the innate immune system is to distinguish between harmless antigens and potentially dangerous pathogens. Ideally, innate immune cells should activate the adaptive immune cells only in the case of invading pathogens. The evolutionarily rather new adaptive immune system, which can be found in jawed fish and higher vertebrates, needs several days to mount an efficient response upon its first encounter with a certain pathogen. As soon as antigen-specific lymphocyte clones have been expanded, they powerfully fight the pathogen. Importantly, memory lymphocytes can often protect us from reinfections. During the development of T and B lymphocytes, many millions of different receptors are generated by somatic recombination and hypermutation of gene segments making up the antigen receptors. This process carries the inherent risk of autoimmunity, causing most inflammatory rheumatic diseases. In contrast, inadequate activation of the innate immune system, especially activation of the inflammasomes, may cause autoinflammatory syndromes.

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