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Thematische Bibliographien / Activation/tolérance des lymphocytes T / Bücher

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Bücher zum Thema „Activation/tolérance des lymphocytes T“

Autor: Grafiati

Veröffentlicht am 18. Mai 2024

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1

Charles, Snow E., Hrsg. T-cell dependent and independent B-cell activation. Boca Raton: CRC Press, 1991.

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2

1950-, Grinstein Sergio, und Rotstein Ori D, Hrsg. Mechanisms of leukocyte activation. San Diego: Academic Press, 1990.

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3

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

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4

Branch, Moody D., Hrsg. T cell activation by CD1 and lipid antigens. Berlin: Springer, 2007.

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5

T cell protocols. 2. Aufl. New York: Humana Press, 2009.

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6

Cooper, David. Suppressed PHA activation of T lymphocytes in simulated microgravity is restored by direct activation of protein kinase C with phorbol ester. [Washington, DC: National Aeronautics and Space Administration, 1997.

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7

Cooper, David. Suppressed PHA activation of T lymphocytes in simulated microgravity is restored by direct activation of protein kinase C with phorbol ester. [Washington, DC: National Aeronautics and Space Administration, 1997.

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8

Marc, Feldmann, Maini R. N, Woody James N und United States. Naval Medical Research and Development Command., Hrsg. 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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9

1955-, Suttles Jill, Hrsg. T-cell signaling of macrophage activation: Cell contact-dependent and cytokine signals. Austin: R.G. Landes, 1995.

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10

Jean-Marie, Andrieu, Lu Wei und International Symposium on Cellular Approaches to the Control of HIV Disease (1st : 1994 : Paris, France), Hrsg. Cell activation and apoptosis in HIV infection: Implications for pathogenesis and therapy. New York: Plenum Press, 1995.

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11

Libero, Gennaro De. T Cell Protocols. Humana Press, 2011.

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12

T Cell Protocols: Development and Activation (Methods in Molecular Biology). Humana Press, 2000.

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13

Feldmann, M., und 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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14

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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15

Salmena, Leonardo. Caspase-8 in T-lymphocytes: An effector of apoptosis and modulator of activation-induced proliferation and T-cell immunity. 2005.

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16

Grom, Alexei A., und Athimalaipet V. Ramanan. Macrophage activation syndrome. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0168.

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Macrophage activation syndrome (MAS) is a life-threatening condition caused by excessive activation and proliferation of T lymphocytes and haemophagocytic macrophages. Although MAS has been reported in association with almost any rheumatic disease, it is by far most common in systemic juvenile idiopathic arthritis. Flares of the underlying disease or infection are most common triggers of MAS. The pathognomonic feature of MAS is typically found in bone marrow: numerous, well-differentiated macrophagic histiocytes phagocytosing normal haematopoietic elements. The expansion of these histiocytes leads to a massive systemic inflammatory reaction associated with three cardinal clinical features: severe cytopenias, liver dysfunction, and coagulopathy consistent with disseminated intravascular coagulation. Clinically, MAS is strikingly similar to the autosomal recessive disorders collectively known as familial haemophagocytic lymphohistiocytosis (FHLH). FHLH has been associated with various genetic defects affecting the cytolytic pathway. Cytolytic function is profoundly depressed in MAS patients as well, and this abnormality is caused by both genetic and acquired factors. Studies in animals suggest that uncontrolled expansion of activated CD8+ T lymphocytes secreting cytokines that activate macrophages is central to the pathophysiology of haemophagocytic syndromes. Consistent with this view, the combination of steroids and ciclosporin, an immunosuppressant that preferentially inhibits T lymphocytes, is an effective treatment for the majority of MAS patients. Patients in whom MAS remains active despite this treatment present a serious challenge and require more aggressive immunosuppression. However, in MAS triggered by infection, the optimal level of immunosuppression is difficult to determine. As a result, reported mortality rates reach 20%.

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17

Andrieu, Jean-Marie, und Wei Lu. Cell Activation and Apoptosis in HIV Infection: Implications for Pathogenesis and Therapy. Springer London, Limited, 2012.

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18

(Editor), Jean-Marie Andrieu, und Wei Lu (Editor), Hrsg. Cell Activation and Apoptosis in HIV Infection: Implications for Pathogenesis and Therapy (Advances in Experimental Medicine and Biology). Springer, 1995.

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19

Misbah, Siraj. Immunosuppressive therapy and therapeutic monoclonal antibodies. Herausgegeben von Patrick Davey und 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.

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20

Voll, Reinhard E., und 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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21

Hartigan-O’Connor, Dennis J., und 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.

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22

Moerdler, Scott, und 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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23

Tsai, Ching-Wei, Sanjeev Noel und 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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24

K. Gautam, Rupesh, Lokesh Deb und Kamal Dua, Hrsg. Natural Products for the Management of Arthritic Disorders. BENTHAM SCIENCE PUBLISHERS, 2022. http://dx.doi.org/10.2174/97898150507761220101.

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Rheumatoid arthritis (RA) is the most common inflammatory complication and affects approximately 1 % of the global population. It affects three times more women than men. RA is an autoimmune disorder elicited by exposure of genetic factors from the host to unknown antigens causing arthritogenic complaints. It also includes the activation of lymphocytes as well as CD4+ helper T cells along with local release of chronic inflammatory mediators and cytokines like tumor necrosis factor (TNF α) and various cytokines like interleukins (IL) that enormously affect the joints. The available allopathic therapies for RA are not a cure for the complications, and antibody therapy and surgical procedures are expensive. However, in the present era, researchers and healthcare professionals have moved toward natural medicines obtained from plants and other natural sources. Research based on developments in phytomedicine has progressed steadily. Evidence has been collected to show the massive therapeutic potential of medicinal plants used in various traditional systems against many pathological complications. Researchers have focused on the therapeutic potential of natural products used for treatment and counteracting various disorders along with their complications having negligible adverse effects. Natural Products for the Management of Arthritic Disorders compiles current knowledge about the bioactive compounds and herbal formulations useful in the treatment of rheumatoid arthritis. 11 chapters explain the role of natural products in the management of rheumatoid arthritis. Topics have been contributed by experts in medicinal chemistry and rheumatology. The book first introduces the reader to rheumatoid arthritis before delving into conventional and alternative therapies for the disease. The editors have also included special topics such as the biomarkers for RA, cytokines and anti-inflammatory mediators, preclinical and clinical studies. The range of topics should provide a comprehensive overview of natural remedies for arthritis and the role of natural products in anti-arthritic drug development. The information will be useful for many readers including medical and pharmacology students, multidisciplinary research scholars, scientists, pharma / herbal / food industrialists, and policy makers.

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