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Published: 10 March 2023

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1

Alexander, Michael A. Immune-based cancer treatment: The T lymphocyte response. Boca Raton, FL: CRC Press, 2011.

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2

Alexander, Michael A. Immune-based cancer treatment: The T lymphocyte response. Boca Raton, FL: CRC Press, 2011.

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3

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

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4

H, Kiyono, and McGhee Jerry R, eds. Mucosal immunology: Intraepithelial lymphocytes. New York: Raven Press, 1994.

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5

Rook, G. A. W. 1946- and Lightman Stafford L, eds. Steroid hormones and the T-cell cytokine profile. London: Springer, 1997.

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6

1943-, Watson James D., and Marbrook John, eds. Recognition and regulation in cell-mediated immunity. New York, N.Y: M. Dekker, 1985.

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7

Miami Bio/Technology Winter Symposium (1990 Miami, Fla.). Advances in gene technology: The molecular biology of immune diseases and the immune reponse : proceedings of the 1990 Miami Bio/Technology Winter Symposia. Oxford: IRL Press, 1990.

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8

B, Schook Lawrence, Tew John G, and International RES Symposium (1987 : Richmond, Va.), eds. Antigen presenting cells: Diversity, differentiation, and regulation : proceedings of a symposium held in Richmond, Virginia, March 26-29, 1987. New York: Liss, 1988.

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9

Z, Atassi M., and Abbott Laboratories, eds. Immunobiology of proteins and peptides IV: T-cell recognition and antigen presentation. New York: Plenum Press, 1987.

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10

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

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11

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

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12

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

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13

International Conference on Lymphocyte Activation and Immune Regulation (9th 2002 Newport Beach, Calif.). Lymphocyte activation and immune regulation IX: Homeostasis and lymphocyte traffic. New York: Kluwer Academic/Plenum Publishers, 2002.

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14

Sudhir, Gupta, ed. Mechanisms of lymphocyte activation and immune regulation XI: B cell biology. New York: Springer, 2007.

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15

Brouwenstijn, Nathalie. Characterization of the T-cell mediated immune response to renal cell carcinoma. [Leiden: University of Leiden], 1998.

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16

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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17

D, Batista Facundo, and SpringerLink (Online service), eds. Immunological Synapse. Berlin, Heidelberg: Springer-Verlag Berlin Heidelberg, 2010.

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18

Rao, Samhita Anand. Deconstructing T cell transcriptional heterogeneity and clonal dynamics in response to immune checkpoint blockade. [New York, N.Y.?]: [publisher not identified], 2022.

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19

H, Kiyono, Jirillo E, De Simone Claudio, and International Conference on Molecular Aspects of Immune Response and Infectious Diseases (1989 : Rome, Italy), eds. Molecular aspects of immune response and infectious diseases. New York: Raven, 1990.

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20

Meding, Sally Joanna. CD4(plus) T cell effector mechanisms in the protective immune response to Plasmodium chabaudi chabaudi. Uxbridge: Brunel University, 1991.

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21

Sudhir, Gupta, and International Conference on Mechanisms of Lymphocyte Activation and Immune Regulation (5th : 1994 : Newport Beach, Calif.), eds. Mechanisms of lymphocyte activation and immune regulation V: Molecular basis of signal transduction. New York: Plenum Press, 1994.

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22

Constandinou, Christothea Maria. Clinical phenotypic aspects of T-cell lymphomas and Hodgkin's disease,its association with the Epstein-Barr virus, and its influence on the immune response. Wolverhampton: University of Wolverhampton, 2002.

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23

Killer cell dynamics: Mathematical and computational approaches to immunology. New York, NY: Springer, 2007.

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24

Breban, Maxime, and Hill Gaston. Immune mechanisms: adaptive immunity. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198734444.003.0008.

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The role of adaptive immunity (i.e. the involvement of B and T lymphocytes) in the pathogenesis of axial spondyloarthritis has been investigated in both human disease and relevant animal models. Studies of B cell responses have not generally implicated an autoantibody in the disease, but there are abnormalities of antibody responses, particularly increased titres of antibodies to various gut bacteria. T cells are critical to the disease in animal models other than those where overexpression of a cytokine is engineered, suggesting that they are the drivers of the inflammatory response. There is convergent evidence from animal models, genetics in humans, and direct observation of human peripheral blood and joints to implicate T cells producing IL-17 under the influence of IL-23. These in turn may be responding to bacteria either in the gut or on the skin.
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25

Mucosal Immunology: Intraepithelial Lymphocytes (Advances in Host Defense Mechanisms). Raven Pr, 1994.

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26

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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27

Moerdler, Scott, and Xingxing Zang. PD-1/PDL-1 Inhibitors as Immunotherapy for Ovarian Cancer. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190248208.003.0010.

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Programmed death 1 (PD-1), a member of the B7-CD28 immunoglobulin superfamily, and its ligands PD-L1/PD-L2 inhibit T-cell activation. They also play a key role in the tumor microenvironment, allowing for cancer immune escape. PD-1 is induced on a variety of immune cells, including tumor-infiltrating lymphocytes (TILs), while PD-L1 is found on many types of solid tumors including ovarian cancer and some TILs. The use of immunocheckpoint inhibitors like anti-PD-1 and anti-PD-L1 therapies has been shown to reactivate the immune system to attack tumor cells. Ovarian cancers have been shown to be responsive to anti-PD-1 and anti-PD-L1 therapies, though immunocheckpoint inhibitors are not enough. Current research is evaluating combination therapies to improve response rates.
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28

Atassi, M. Zouhair, and Howard L. Bachrach. Immunobiology of Proteins and Peptides IV: T-Cell Recognition and Antigen Presentation. Springer London, Limited, 2012.

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29

Atassi, M. Zouhair. Immunobiology of Proteins and Peptides Iv: T-Cell Recognition And Antigen Presentation. Springer, 2012.

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30

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

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31

Muthukumar, Thangamani, Darshana Dadhania, Choli Hartono, and Manikkam Suthanthiran. Immunology, sensitization, and histocompatibility. Edited by Jeremy R. Chapman. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0279.

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Allograft rejection of the histo-incompatible allograft involves a highly orchestrated action of multiple cell types and mediators, with lymphocytes responsible for the identification of the foreignness of the allograft. The immune response directed against the donor is primarily, but not exclusively, directed at the donor’s major histocompatibility complex region class I and class II proteins. This chapter describes the immunobiology of the T cell and the role of human leucocyte antigens in clinical transplantation, thus identifying the targets for manipulation of the immune response by immune suppressants and through strategies designed to create a state of tolerance of the allograft.
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32

(Editor), Dirk Nagorsen, and F. M. Marincola (Editor), eds. Analyzing T Cell Responses: How to analyze cellular immune responses against tumor associated antigens. Springer, 2005.

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33

Marincola, Francesco M., and Dirk Nagorsen. Analyzing T Cell Responses: How to Analyze Cellular Immune Responses Against Tumor Associated Antigens. Springer London, Limited, 2006.

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34

Marincola, Francesco M., and Dirk Nagorsen. Analyzing T Cell Responses: How to Analyze Cellular Immune Responses Against Tumor Associated Antigens. Springer, 2010.

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35

Tsai, Ching-Wei, Sanjeev Noel, and 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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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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36

Gupta, Sudhir, and J. John Cohen. Mechanisms of Lymphocyte Activation and Immune Regulation VI: Cell Cycle and Programmed Cell Death in the Immune System. Springer, 2013.

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37

Alt, Frederick W., Fritz Melchers, Sudhir Gupta, Max D. Cooper, and Klaus Rajewsky. Mechanisms of Lymphocyte Activation and Immune Regulation XI: B Cell Biology. Springer, 2010.

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38

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

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39

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

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40

Lightman, S., and G. A. W. Rook. Steroid Hormones and the T-Cell Cytokine Profile. Springer London, Limited, 2011.

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41

Lightman, S., and G. A. W. Rook. Steroid Hormones and the T-Cell Cytokine Profile. Springer London, Limited, 2012.

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42

Go, Cynthia. IL-2 gene regulation during T cell activation and anergy induction. 1992.

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43

McKisic, Maureen Denise. Characterization of ova-reactive and alloreactive CD4+ T cell subsets. 1992.

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44

(Editor), Sudhir Gupta, Frederick W. Alt (Editor), Max D. Cooper (Editor), Fritz Melchers (Editor), and Klaus Rajewsky (Editor), eds. Mechanisms of Lymphocyte Activation and Immune Regulation XI: B Cell Biology (Advances in Experimental Medicine and Biology). Springer, 2007.

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45

(Editor), Sudhir Gupta, Eugene Butcher (Editor), and William E. Paul (Editor), eds. Lymphocyte Activation and Immune Regulation IX: Homeostasis and Lymphocyte Traffic (Advances in Experimental Medicine and Biology). Springer, 2007.

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46

Cellular basis of immune modulation: Proceedings of the 19th International Leukocyte Culture Conference held at Banff Springs Hotel, Banff, Alberta, May 8-12, 1988 (Progress in leukocyte biology). A.R. Liss, 1988.

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47

Atassi, M. Zouhair, and Howard L. Bachrach. Immunobiology of Proteins and Peptides (Advances in Experimental Medicine and Biology). Springer, 1988.

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48

Howard, Colin R. Arenaviruses. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0032.

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There are few groups of viral zoonoses that have attracted such widespread publicity as the arenaviruses, particularly during the 1960’s and 1970’s when Lassa emerged as a major cause of haemorrhagic disease in West Africa. More than any other zoonoses, members of the family are used extensively for the study of virus-host relationships. Thus the study of this unique group of enveloped, single-stranded RNA viruses has been pursued for two quite separate reasons. First, lymphocytic choriomeningitis virus (LCM) has been used as a model of persistent virus infections for over half a century; its study has contributed, and continues to contribute, a number of cardinal concepts to our present understanding of immunology. LCM virus remains the prototype of the Arenaviridae and is a common infection of laboratory mice, rats and hamsters. Once thought rare in humans there is now increasing evidence of LCM virus being implicated in renal disease and as a complication in organ transplantation. Second, certain arenaviruses cause severe haemorrhagic diseases in man, notably Lassa fever in Africa, Argentine and Bolivian haemorrhagic fevers in South America, Guaranito infection in Venezuela and Chaparé virus in Bolivia. The latter is a prime example for the need of ever-continuing vigilance for the emergence of new viral diseases; over the past few years several new arenaviruses have been reported as implicated with severe human disease and indeed the number of new arenaviruses discovered since the last edition of this book have increased the size of this virus family significantly.In common with LCM, the natural reservoir of these infections is a limited number of rodent species (Howard, 1986). Although the initial isolates from South America were at first erroneously designated as newly defined arboviruses, there is no evidence to implicate arthropod transmission for any arenavirus. However, similar methods of isolation and the necessity of trapping small animals have meant that the majority of arenaviruses have been isolated by workers in the arbovirus field. A good example of this is Guaranito virus that emerged during investigation of a dengue virus outbreak in Venezuela (Salas et al. 1991).There is an interesting spectrum of pathological processes among these viruses. All the evidence so far available suggests that the morbidity of Lassa fever and South American haemorrhagic fevers due to arenavirus infection results from the direct cytopathic action of these agents. This is in sharp contrast to the immunopathological basis of ‘classic’ lymphocytic choriomeningitis disease seen in adult mice infected with LCM virus and the use of this system for elucidating the phenomenon of H2-restriction of the host cytotoxic T cell response (Zinkernagel and Doherty 1979). Despite the utility of this experimental model for dissecting the nature of the immune response to virus infection and the growing interest in arenaviruses of rodents, there remains much to be done to elucidate the pathogenesis of these infections in humans.
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49

Wodarz, Dominik. Killer Cell Dynamics: Mathematical and Computational Approaches to Immunology. Springer, 2010.

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50

Killer Cell Dynamics: Mathematical and Computational Approaches to Immunology. Springer London, Limited, 2007.

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