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Готові списки джерел за темами / Immune cell activation / Книги

Книги з теми "Immune cell activation"

Щоб переглянути інші типи публікацій з цієї теми, перейдіть за посиланням: Immune cell activation.

Автор: Grafiati

Опубліковано: 7 липня 2024

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1

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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2

International Conference on B Cell Biology (11th 2006 Newport Beach, Calif.). Mechanisms of lymphocyte activation and immune regulation XI: B cell biology. New York: Springer, 2007.

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3

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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4

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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5

David, Naor, ed. Receptor activation by antigens, cytokines, hormones, and growth factors. New York, N.Y: New York Academy of Sciences, 1995.

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6

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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7

Marc, Feldmann, Maini R. N, Woody James N, and United States. Naval Medical Research and Development Command., eds. T-cell activation in health and disease: Disorders of immune regulation infection and autoimmunity : papers from an international meeting in Oxford, UK, in September 1988. London ; San Diego: Academic Press, 1989.

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8

International Conference on Lymphocyte Activation and Immune Regulation (1986 Newport Beach, Calif.). Mechanisms of lymphocyte activation and immune regulation. New York: Plenum Press, 1987.

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9

International Conference on Lymphocyte Activation and Immune Regulation (1986 Newport Beach, Calif.). Mechanisms of lymphocyte activation and immune regulation. New York: Plenum Press, 1987.

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10

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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11

Waldmann, Thomas, and Sudhir Gupta. Mechanisms of lymphocyte activation and immune regulation IV: Cellular communications. New York: Springer Science+Business Media, 1992.

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12

Sudhir, Gupta, Sher Alan, Ahmed Rafi, and International Conference on Lymphocyte Activation and Immune Regulation (7th : 1998 : Newport Beach, Calif.), eds. Mechanisms of lymphocyte activation and immune regulation VII: Molecular determinants of microbial immunity. New York: Plenum Press, 1998.

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13

Regueiro, José R. Human T-lymphocyte activation deficiencies. Austin, TX: R.G. Landes, 1994.

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14

(Editor), Sudhir Gupta, and J. John Cohen (Editor), eds. Mechanisms of Lymphocyte Activation and Immune Regulation Vi: Cell Cycle and Programmed Cell Death in the Immune System. Springer, 1996.

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15

Mechanisms of lymphocyte activation and immune regulation VI: Cell cycle and programmed cell death in the immune system. New York: Plenum Press, 1996.

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16

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 London, Limited, 2013.

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17

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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18

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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19

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

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20

Oxidative stress, cell activation and viral infection. Basel: Birkhäuser Verlag, 1994.

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21

Azuma, Miyuki, and Hideo Yagita. Co-signal Molecules in T Cell Activation: Immune Regulation in Health and Disease. Springer, 2019.

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22

Azuma, Miyuki, and Hideo Yagita. Co-Signal Molecules in T Cell Activation: Immune Regulation in Health and Disease. Springer Singapore Pte. Limited, 2020.

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23

(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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24

(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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25

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.

26

Jay, Taylor R., Shane M. Bemiller, Lee E. Neilson, Paul J. Cheng-Hathaway, and Bruce T. Lamb. Neuroinflammation and Neurodegenerative Diseases. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0004.

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Neuroinflammation has long been associated with many neurodegenerative diseases (NDDs). Immune-related genetic and environmental risk factors have recently been identified for NDDs, suggesting that neuroinflammation can play an active role in modifying NDD pathologies. Immune cells that underlie this neuroinflammatory response can have both beneficial and detrimental roles in NDDs. These cells can engage in clearance of debris and provide important survival factors to neighboring neurons. However, these cells can also release inflammatory molecules that promote oxidative stress and excitotoxic damage in surrounding neurons, and aberrantly clear healthy cells and structures from the brain. In turn, the cells within the brain play important roles in determining the phenotype and function of these immune cells, and changes in the interaction among these cells in the context of disease can lead to detrimental immune cell activation. There has been recent interest in developing inflammation-related biomarkers to help diagnose NDDs and immune-targeted therapeutics.

27

Feldmann, M., and R. Maini. T-Cell Activation in Health and Disease Disorders of Immune Regulation Infection and Autoimmunity: Papers from an International Meeting in Oxford, U. Academic Press, 1989.

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28

Hartigan-O’Connor, Dennis J., and Christian Brander. Immunology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190493097.003.0005.

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The key factor in HIV pathogenesis is the decline in CD4+ T cells with resultant immunodeficiency and chronic inflammation. Depletion of CD4+ T cells from the gastrointestinal mucosa followed by microbial translocation and subsequent immune activation are components of disease progression in untreated patients. Symptomatic and occult opportunistic infections including cytomegalovirus contribute to chronic inflammation in persons infected with HIV. Antiretroviral therapy (ART) results in immune reconstitution, with increases in peripheral CD4+ T cell lymphocytes in most persons infected with HIV, although immune recovery is quite variable. A subset of patients with AIDS will develop immune reconstitution inflammatory syndromes after initiation of ART. Approximately 1% of persons with HIV are able to control infection without the need for ART (“elite” controllers). A variety of immune-based therapies, including hydroxyurea, growth hormone, and statins, are being studied in clinical trials and may ultimately play a role in treating persons with HIV infection.

29

Yee, Chee-Seng. Systemic lupus erythematosus. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0269.

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Systemic lupus erythematosus is a chronic multisystem autoimmune inflammatory disorder of unknown etiology. Numerous abnormalities within the innate and adaptive immune system have been described. The hallmark of this disease is B-cell hyperactivity resulting in autoantibody production, abnormal T-cell function, impaired clearance of immune complexes (resulting in their deposition in tissues), complement activation, and defective cellular apoptosis. However, these abnormalities of the immune system are not uniform across patients or within the same patient at different stages of the disease, resulting in heterogeneity in its presentation and progress.

30

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.

31

Woody, J. N., M. Feldmann, and R. Maini. T-Cell Activation in Health and Disease : Disorders of Immune Regulation Infection and Autoimmunity: Papers from an International Meeting in Oxford, UK, in September 1988. Elsevier Science & Technology Books, 2017.

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32

T-cell activation in health and disease: Disorders of immune regulation : infection and autoimmunity : papers from an international meeting in Oxford, UK, in September 1988. London: Academic Press, 1989.

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33

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

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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.

34

Misbah, Siraj. Immunosuppressive therapy and therapeutic monoclonal antibodies. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0302.

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The term immunosuppressive therapy encompasses all forms of treatment that dampens function of the recipient’s immune system, with a view to controlling severe autoimmune, inflammatory, or allergic disease. The predominant targets of these agents are T-lymphocytes with multiple downstream effects, including containment of T-cell activation, inhibition of cytokine production, restriction of clonal expansion, and varying degrees of suppression of B-cell function. This chapter reviews the clinical use of monoclonal antibodies and other immunosuppressive agents, and their mechanisms of action.

35

Dambuza, Ivy M., Jeanette Wagener, Gordon D. Brown, and Neil A. R. Gow. Immunology of fungal disease. Edited by Christopher C. Kibbler, Richard Barton, Neil A. R. Gow, Susan Howell, Donna M. MacCallum, and Rohini J. Manuel. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755388.003.0009.

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Advances in modern medicine, such as organ transplantations and the appearance of HIV (human immunodeficiency virus), have significantly increased the patient cohort at risk of developing chronic superficial and life-threatening invasive fungal infections. To tackle this major healthcare problem, there is an urgent need to understand immunity against fungal infections for the purposes of vaccine design or immune-mediated interventions. In this chapter, we give an overview of the components of the innate and adaptive immune system and how they contribute to host defence against fungi. The various cell types contributing to fungal recognition and the subsequent stimulation of phagocytosis, the activation of inflammatory and B- and T-cell responses, and fungal clearance are discussed using the major fungal pathogens as model systems.

36

Braquet. Platelet-activating Factor Cell Immuno. Karger, 1988.

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37

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.

38

Paul, William E., Sudhir Gupta, and Eugene Butcher. Lymphocyte Activation and Immune Regulation IX: Homeostasis and Lymphocyte Traffic. Springer, 2012.

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39

Paul, William E., Sudhir Gupta, and Eugene Butcher. Lymphocyte Activation and Immune Regulation IX: Homeostasis and Lymphocyte Traffic. Springer London, Limited, 2012.

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40

Monaco, Claudia, and Giuseppina Caligiuri. Molecular mechanisms. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0014.

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The development of the atherosclerotic plaque relies on specific cognate interactions between ligands and receptors with the ability to regulate cell recruitment, inflammatory signalling, and the production of powerful inflammatory and bioactive lipid mediators. This chapter describes how signalling is engaged by cell-cell surface interactions when the endothelium interacts with platelets and leukocytes enhancing leukocyte recruitment during atherogenesis. It also exemplifies intracellular signalling pathways induced by the activation of innate immune receptors, the most potent activators of inflammation in physiology and disease. Differences are highlighted in innate signalling pathways in metabolic diseases such as atherosclerosis compared to canonical immunological responses. Finally, the key lipid mediators whose production can affect endothelial function, inflammation, and atherosclerosis development are summarized. This Chapter will take you through these fundamental steps in the development of the atherosclerotic plaque by summarizing very recent knowledge in the field and highlighting recent or ongoing clinical trials that may enrich our ability to target cardiovascular disease in the future.

41

Fauci, Anthony, Sudhir Gupta, and William E. Paul. Mechanisms of Lymphocyte Activation and Immune Regulation. Springer, 2012.

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42

Fauci, Anthony, William E. Paul, and Sudhir Gupta. Mechanisms of Lymphocyte Activation and Immune Regulation. Springer London, Limited, 2013.

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43

(Editor), M. D. Cooper, T. Takai (Editor), and J. V. Ravetch (Editor), eds. Activating and Inhibitory Immunoglobulin-like Receptors. Springer, 2001.

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44

Fleischmann, Roy. Signalling pathway inhibitors. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0081.

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Oral, small-molecule signalling pathway inhibitors, including ones that inhibit the JAK and SyK pathways, are currently in development for the treatment of rheumatoid arthritis (RA). Tofacitinib is an orally administered small-molecule inhibitor that targets the intracellular Janus kinase 3 and 1 (JAK1/3) molecules to a greater extent than JAK2 while baricitinib (formerly INCB028050) predominantly inhibits JAK1/2. Many of the proinflammatory cytokines implicated in the pathogenesis of RA utilize cell signalling that involves the JAK-STAT pathways and therefore inhibition of JAK-STAT signalling, by targeting multiple RA-associated cytokine pathways, has the potential to simultaneously reduce inflammation, cellular activation, and proliferation of key immune cells. Fostamatinib disodium is an orally available inhibitor of spleen tyrosine kinase (SyK), which is a cytoplasmic tyrosine kinase that is an important mediator of immunoreceptor signalling in mast cells, macrophages, neutrophils, and B cells. Interruption of SyK signalling may interrupt production of tumour necrosis factor (TNF) and metalloproteinase and therefore affect RA disease activity. Tofacitinib has been investigated in multiple phase 2 and phase 3 trials which have investigated its efficacy (clinical, functional, and radiographic) and safety in patients who have failed disease-modifying anti-inflammatory drugs (DMARDs) as monotherapy or in combination with DMARDs, compared to an inhibitor of tumour necrosis factor alpha (TNFα‎) and in patients who have failed TNFα‎ inhibitors. The efficacy of fostamatinib and baricitinib has been investigated in phase 2 trials; both are in large phase 3 clinical programmes. Each of these medications has demonstrated efficacy; their safety profile has been shown to be different from each other and from currently approved biological agents. This chapter discusses what is currently known and understood about their efficacy and safety.

45

Ahmed, Rafi, Sudhir Gupta, and Alan Sher. Mechanisms of Lymphocyte Activation and Immune Regulation VII: Molecular Determinants of Microbial Immunity. Springer London, Limited, 2012.

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46

Josephs, Debra H., Heather J. Bax, Giulia Pellizzari, James F. Spicer, Ana Montes, and Sophia N. Karagiannis. Antibody Therapeutics for Ovarian Carcinoma and Translation to the Clinic. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190248208.003.0001.

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Despite improvements over the past decade in the treatment of ovarian cancer, many patients are at risk of recurrent disease and emerging drug resistance. The increased selectivity and reduced toxicity of molecularly targeted anti-cancer agents renders them attractive for development in ovarian cancer, and monoclonal antibodies targeting ovarian cancer-specific tumor antigens represent the largest such group investigated in this clinical setting. This chapter describes examples of monoclonal antibodies clinically evaluated for efficacy in ovarian cancer. These agents recognize molecular targets expressed on tumors or within tumor microenvironments that may be essential for tumor cell survival and proliferation. Recently, antibodies targeting checkpoint molecules on immune cells have shown efficacy in modulating anti-tumor immunity, and applications in ovarian carcinomas are evaluated. The chapter focuses on therapeutic agents’ attributes on targeting key cancer growth and progression pathways, and propensity to engender effector functions by activating immune effector cells in tumors and the circulation.

47

Ahmed, Rafi, Sudhir Gupta, and Alan Sher. Mechanisms of Lymphocyte Activation and Immune Regulation VII: Molecular Determinants of Microbial Immunity. Springer London, Limited, 2012.

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48

(Editor), Sudhir Gupta, Alan Sher (Editor), and Rafi Ahmed (Editor), eds. Mechanisms of Lymphocyte Activation and Immune Regulation Vii: Molecular Determinants of Microbial Immunity. Springer, 1998.

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49

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.

50

Lloyd, Peter, Sarah Doaty, and Bevra H. Hahn. Aetiopathogenesis of systemic lupus erythematosus. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198739180.003.0002.

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Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by the presence of immune dysregulation, autoreactive B and T cells, and the production of a broad, heterogeneous group of autoantibodies (autoAb). The pathogenesis of lupus can be divided into three stages: 1) genetic predisposition and environmental exposures, 2) loss of tolerance, and 3) immune activation. In this chapter we will discuss the aetiopathogenesis of systemic lupus erythematosus with emphasis placed on key autoantibodies, cytokines, the innate and adaptive immune system, tolerance, NETosis, genetics and epigenetics, environmental triggers and the role of gender.