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Готові списки джерел за темами / Immune system genes / Книги

Книги з теми "Immune system genes"

Щоб переглянути інші типи публікацій з цієї теми, перейдіть за посиланням: Immune system genes.

Автор: Grafiati

Опубліковано: 10 грудня 2022

Оновлено: 28 січня 2023

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1

Fox, C. Fred, Eli E. Sercarz, and Alan R. Williamson. Immune System: Genes, Receptors, Signals. Elsevier Science & Technology Books, 2013.

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2

Cantor, Harvey, Leonard Chess, and Eli E. Sercarz. Regulation of the Immune System. Wiley & Sons, Incorporated, John, 1985.

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3

Radtke, Freddy. Notch Regulation of the Immune System. Springer London, Limited, 2012.

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4

Radtke, Freddy. Notch Regulation of the Immune System. Springer Berlin / Heidelberg, 2014.

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5

Notch Regulation Of The Immune System. Springer, 2012.

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6

(Editor), Y. Becker, and Gholamreza Darai (Editor), eds. Molecular Evolution of Viruses - Past and Present: Evolution of Viruses by Acquisition of Cellular RNA and DNA (VIRUS GENES). Springer, 2007.

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7

Becker, Yechiel. Molecular Evolution of Viruses - Past and Present: Evolution Of Viruses By Acquisition Of Cellular Rna And Dna. Springer, 2012.

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8

Yechiel, Becker, and Darai Gholamreza, eds. Molecular evolution of viruses-past and present: Evolution of viruses by acquisition of cellular RNA and DNA. Boston: Kluwer Academic Publishers, 2000.

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9

Becker, Yechiel. Molecular Evolution of Viruses - Past and Present. Springer, 2011.

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10

Becker, Yechiel, and Gholamreza Darai. Molecular Evolution of Viruses -- Past and Present: Evolution of Viruses by Acquisition of Cellular RNA and DNA. Springer London, Limited, 2012.

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11

Becker, Yechiel. Molecular Evolution of Viruses -- Past and Present. Springer London, Limited, 2012.

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12

JESSBERGER. Molecular Analysis Of Dna Rearrangements In The Immune System (Current Topics in Microbiology & Immunology). SPRINGER-VERLAG, 1996.

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13

Davis, William C., J. N. Shelton, and C. W. Weems. Characterization of the Bovine Immune System and the Genes Regulating Expression of Immunity With Particular Reference to Their Role in Disease resist. Washington State Univ College of, 1986.

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14

Rogler, Gerhard. Gastrointestinal system. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0021.

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Rheumatic diseases and diseases of the gastrointestinal (GI) tract are connected in two ways. The extraintestinal manifestations of inflammatory GI diseases such as inflammatory bowel disease affect joints in up to one-third of patients. On the other hand, several rheumatic diseases such as vasculitis or systemic lupus erythematosus (SLE) induce a wide spectrum of gastrointestinal manifestations. The GI tract constitutes a huge area in contact with the environment. It is exposed to billions of food antigens, commensal bacteria, and potential pathogens. Some of those antigens are thought to play a role in the pathogenesis of rheumatic diseases. The intestinal barrier function and the gut immune system are tightly regulated, as on one hand tolerance for food antigens and the resident commensal flora needs to be maintained, and on the other hand pathogens need to be rapidly and effectively eliminated. Non-infectious, chronic inflammatory diseases of the small and large intestine with rheumatic manifestations have been well known for decades. Among the susceptibility genes for Crohn's disease and ulcerative colitis are some that also cause susceptibility to rheumatoid arthritis or SLE, indicating a shared susceptibility and overlapping pathological mechanisms. Subsequently, similar therapeutic principles have successfully been applied in autoimmune GI and rheumatological diseases such as steroids, immunosuppressants, and anti-TNF (tumour necrosis factor) antibodies.

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15

C, Davis W., Shelton J. N, Weems C. W, and Washington State University. Dept. of Veterinary Microbiology and Pathology., eds. Characterization of the bovine immune system and the genes regulating expression of immunity with particular reference to their role in disease resistance: Proceedings from a symposium held May 1-5, 1984 at the East-West Center, Honolulu, Hawaii. Pullman, Wash: Dept. of Veterinary Microbiology and Pathology, College of Veterinary Medicine, Washington State University, 1985.

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16

Fabbri, Chiara, and Alessandro Serretti. The treatment of bipolar disorder in the era of personalized medicine: myth or promise? Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198748625.003.0031.

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Bipolar disorder (BD) is a chronic disease associated with high personal and socio-economic burden. Genetics accounts for 20–95% of variability in central nervous system drug disposition and pharmacodynamics, thus genetic markers are considered a promising way to develop tailored treatments and improve the prognosis of the disease. Among mood stabilizers, lithium response was the most investigated phenotype and the most replicated genes are involved in synaptic plasticity (BDNF), serotonergic (SLC6A4) and dopaminergic (DRD1) neurotransmission, and second messenger cascades (GSK3B). Relevant pharmacogenetic findings regarding other mood stabilizers are hyperammonaemia (CPS1 gene) and hepatic dysfunction (POLG gene) induced by valproate and immune-mediated cutaneous hypersensitivity reactions (HLA-B*1502) induced by lamotrigine or carbamazepine. Polymorphisms in cytochrome (CYP) P450 genes are expected to provide useful information particularly in case of polypharmacy. Despite few pharmacogenetic tests are currently recommended, the development of pharmacogenetics in other fields of medicine provides an encouraging perspective.

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17

Sousek, Alexandra, and Mehdi Tafti. The genetics of sleep. Edited by Sudhansu Chokroverty, Luigi Ferini-Strambi, and Christopher Kennard. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199682003.003.0005.

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Although there is strong evidence for a genetic contribution to inter-individual variations in sleep, the underlying factors and their interaction remain largely elusive. Much effort has been expended in studying genetic variations contributing to circadian and sleep phenotypes, the individual pattern of the human sleep EEG, reactions to sleep loss, and the pathophysiology of sleep-related disorders. Certain sleep-related diseases may be caused by single genes, while the etiology of others seems to be variable and complex. This is especially the case when the immune system is involved. This chapter reports on twin and familial studies, genetic variations and mutations affecting neurotransmitters and other signaling pathways and thereby affecting sleep, and impacts of gene expression processes and the immune system on sleep. Although much knowledge has been gained, further research is needed to elucidate the all-embracing mechanisms and their interactions that regulate sleep.

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18

(Editor), Walter Doerfler, and Petra Böhm (Editor), eds. Adenoviruses: Model and Vectors in Virus Host Interactions: Immune System, Oncogenesis, Gene Therapy (Current Topics in Microbiology and Immunology). Springer, 2003.

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19

Signaling & Gene Expression in the Immune System (Cold Spring Harbor Symposia on Quantitative Biology). Cold Spring Harbor Laboratory Press, 2000.

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20

Harbor, Cold Spring. Signaling and Gene Expression in the Immune System (Cold Spring Harbor Symposia on Quantitative Biology). Cold Spring Harbor Laboratory Press, 2000.

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21

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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22

Barros, Rodrigo José Saraiva de, Tereza Cristina de Brito Azevedo, Carla de Castro Sant’Anna, Marianne Rodrigues Fernandes, Leticia Martins Lamarão, and Rommel Mario Rodríguez Burbano. Grupos sanguíneos e anticorpos anti-eritrocitários de importância transfusional. Brazil Publishing, 2020. http://dx.doi.org/10.31012/978-65-5861-112-7.

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Immunohematology is an area dedicated to the study of the interactions of the immune system and blood cells in transfusion practice. Blood transfusion is a therapeutic technique that has been widely used since the 17th century. The transfusion medicine aims to repair the pathological needs of blood components in the living organism, be it red blood cells, plasma, platelets, clotting factors, among others. Despite being a therapeutic means, transfusion of blood components can be considered at risk because it is a biological material and due to the transfusion immunological reactions that can be caused during or after the moment of transfusion. In the surface structure of red blood cells, numerous molecules of a protein, glycoprotein or glycolipid nature are found, which are also called membrane antigens that make up structures and perform transport functions, as receptors, as adhesion, enzymatic and / or complement regulatory molecules. The formation of these antigens occurs by an approximate amount of 39 genes involved in their production, of which 282 different antigens are organized in more than 30 blood group systems. This antigenic diversity is a major cause of the formation of irregular anti-erythrocyte antibodies. Therefore, with the increase in blood transfusions in surgeries, transplants and clinical treatment of cancer and other chronic diseases, a significant increase in the occurrence of alloimmunizations in polytransfused patients began to be observed. Such biological phenomena motivated us to carry out this study and the antigenic diversity motivated us to elaborate this small compendium where we also describe the main blood groups.

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23

Juelg, Boris, and Rajesh Gandhi. HIV Cure Strategies. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190493097.003.0006.

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Although current antiretroviral therapy (ART) is highly effective at controlling HIV-1 replication, it does not eradicate or cure the infection. HIV-1 persists quiescently in cellular reservoirs, not detected by the immune system due to the lack of active viral replication; these reservoirs represent the major obstacle for cure approaches. Reversal of HIV-1 latency and induction of virus expression by a variety of interventions may render infected cells susceptible to immune recognition and active clearance. Strategies to boost immune responses via vaccination, immunomodulation, or gene therapy are being evaluated with the aim of achieving HIV-1 control without antiretroviral therapy, if not viral eradication.

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24

Bittner, Edward A., and Shawn P. Fagan. The host response to trauma and burns in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0304.

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Following severe traumatic injury, patients enter a state of immune dysregulation consisting of both exaggerated inflammation and immune suppression. Traditionally, the host response has been viewed as an early systemic inflammatory response syndrome (SIRS) followed temporally by a compensatory anti-inflammatory or immune-suppressive response syndrome (CARS). While this paradigm has been widely accepted across both medical and scientific fields, recent advances have challenged this concept. The Glue grant investigators recently characterized both the initial inflammatory response to injury and the dynamic evolving recovery process. They found: (1) severe injury produces a rapid (< 12 hours) genomic reprioritization in which 80% of the leukocyte transcriptome is altered; (2) similarities in gene expression patterns between different injuries reveal an apparently fundamental response to severe inflammatory stress, which is far more common than different; (3) alterations in the expression of classical inflammatory and anti-inflammatory as well as adaptive immunity genes occur simultaneously, not sequentially after severe injury; (4) the temporal nature of the current SIRS/CARS paradigm is not supported at the level of the leukocyte transcriptome. Complications are not associated with genomic evidence of a ‘second hit’ and differ only in the magnitude and duration of this genomic reprioritization. Furthermore, the delayed clinical recovery with organ injury is not associated with dramatic qualitative differences in the leukocyte transcriptome. Finally, poor correlation between human and rodent inflammatory genomic responses will alter how the host response is studied in the future.

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25

Lewis, Myles, and Tim Vyse. Genetics of connective tissue diseases. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0042.

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The advent of genome-wide association studies (GWAS) has been an exciting breakthrough in our understanding of the genetic aetiology of autoimmune diseases. Substantial overlap has been found in susceptibility genes across multiple diseases, from connective tissue diseases and rheumatoid arthritis (RA) to inflammatory bowel disease, coeliac disease, and psoriasis. Major technological advances now permit genotyping of millions of single nucleotide polymorphisms (SNPs). Group analysis of SNPs by haplotypes, aided by completion of the Hapmap project, has improved our ability to pinpoint causal genetic variants. International collaboration to pool large-scale cohorts of patients has enabled GWAS in systemic lupus erythematosus (SLE), systemic sclerosis and Behçet's disease, with studies in progress for ANCA-associated vasculitis. These 'hypothesis-free' studies have revealed many novel disease-associated genes. In both SLE and systemic sclerosis, identified genes map to known pathways including antigen presentation (MHC, TNFSF4), autoreactivity of B and T lymphocytes (BLK, BANK1), type I interferon production (STAT4, IRF5) and the NFκ‎B pathway (TNIP1). In SLE alone, additional genes appear to be involved in dysregulated apoptotic cell clearance (ITGAM, TREX1, C1q, C4) and recognition of immune complexes (FCGR2A, FCGR3B). Future developments include whole-genome sequencing to identify rare variants, and efforts to understand functional consequences of susceptibility genes. Putative environmental triggers for connective tissue diseases include infectious agents, especially Epstein-Barr virus; cigarette smoking; occupational exposure to toxins including silica; and low vitamin D, due to its immunomodulatory effects. Despite numerous studies looking at toxin exposure and connective tissue diseases, conclusive evidence is lacking, due to either rarity of exposure or rarity of disease.

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26

Divan, Aysha, and Janice A. Royds. 5. Molecular interactions. Oxford University Press, 2016. http://dx.doi.org/10.1093/actrade/9780198723882.003.0005.

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Every nucleated diploid cell in the body, with the exception of B and T cells of the immune system, has the same genome as its originating single fertilized egg. During development, this single cell differentiates into a complex multicellular organism composed of various cells and tissues each carrying out specialized functions. Although each cell contains a genome of data it needs to select the relevant information from this genetic blueprint to fulfil its own specific function. ‘Molecular interactions’ shows that proteins must be produced in the right place and at the right time. This requires regulation of gene expression in conjunction with a myriad of bio-molecular interactions to coordinate this.

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27

Frenkel, Joost, and Hans R. Waterham. Mevalonate Kinase Deficiency. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0039.

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Mevalonate kinase deficiency (MKD) is an autosomal recessive inborn error of isoprenoid biosynthesis, a pathway yielding sterols and nonsterol isoprenoids.In patients, the enzyme activity of mevalonate kinase is severely reduced due to mutations in the encoding gene, MVK. The substrate, mevalonate, accumulates and is elevated in blood and urine. Shortage of certain downstream products of the pathway, nonsterol isoprenoids, leads to dysregulation of the innate immune system, activation of inflammasomes, and interleukin (IL)-1 mediated inflammation.Symptoms start in early childhood with recurrent attacks of fever, vomiting, diarrhea, headache, sore throat, abdominal pain, arthralgias, painful lymphadenopathy, hepatosplenomegaly, skin rash, and mucosal ulcers. Severely affected patients have additional symptoms, such as intellectual impairment, progressive cerebellar ataxia, and tapetoretinal degeneration. Complications include intestinal obstruction, AA-amyloidosis, hemophagocytosis, and severe infection.Management of MKD is directed at controlling inflammation.

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28

Messacar, Kevin, and Mark J. Abzug. Enterovirus and Parechovirus. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190604813.003.0003.

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Enteroviruses (EVs) comprise a genus in the Picornaviridae family. They are single-stranded RNA viruses and are common causes of human infection. Polioviruses, the prototypic EVs, were historically responsible for widespread outbreaks of paralytic poliomyelitis; now they are on the verge of global elimination through vaccination. More than 100 serotypes of nonpoliovirus EVs are described and are associated with a wide variety of diseases, ranging from respiratory infections, nonspecific febrile illnesses, herpangina, and hand-foot-and-mouth disease to meningitis, encephalitis, paralytic disease, myocarditis, chronic or disseminated infection in immunocompromised hosts (particularly those with defects in the humoral immune response), and severe disease in neonates. This chapter reviews disease manifestations during pregnancy and in neonates, with an emphasis on clinical presentation, diagnosis, and management. The newly emerging parechoviruses, important causes of central nervous system (CNS) disease, are also reviewed.

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29

Thomas, Ranjeny, and Andrew P. Cope. Pathogenesis of rheumatoid arthritis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0109.

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In depth molecular and cellular analysis of synovial tissue and fluid from patients with rheumatoid arthritis has provided important insights into understanding disease pathogenesis. Advances in the 1980s and 1990s included modern cloning strategies, sensitive and specific assays for inflammatory mediators, production of high-affinity neutralizing monoclonal antibodies, advances in flow cytometry, and gene targeting and transgenic strategies in rodents. In the 21st century, technological platforms offer unparalleled opportunities for systematic and unbiased interrogation of the disease process at a whole-genome level. Here we describe the key molecular and cellular characteristics of the inflamed synovium and how infiltrating cells get there. With this background, we outline current concepts of the different phases of disease, how the first phase of genetic susceptibility evolves into autoimmunity, triggered by the exposome, prior to the onset of clinically apparent inflammatory disease. We then describe the pathways that actively contribute to this early inflammatory phase and document the key effector cells and molecules of the innate and adaptive immune systems that orchestrate and maintain chronic synovial inflammatory responses. We summarize how this inflammatory milieu translates to cartilage destruction and bone resorption in synovial joints, and conclude by reviewing those factors in inflamed synovium that promote immune homeostasis.

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30

Aktor, Mikael. Social Classes. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198702603.003.0005.

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The notions of class (varṇa) and caste (jāti) run through the Dharmaśāstra literature on all levels. They regulate marriage, economic transactions, work, punishment, penance, entitlement to rituals, identity markers like the sacred thread, and social interaction in general. Although this social structure was ideal in nature and not equally confirmed in other genres of ancient and medieval literature, it has nevertheless had an immense impact on Indian society. The chapter presents an overview of the system with its three privileged classes, the Brahmins, the Kṣatriyas, and the Vaiśyas, the fourth underprivileged class, the Śūdras, and, at the bottom of the society, the lowest so-called untouchable castes. It also discusses the understanding of human differences that lies at the center of the system and the possible economic and political motivations of the Brahmin authors of the texts.

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31

Harvey, Mark S. Catalogue of the Smaller Arachnid Orders of the World. CSIRO Publishing, 2003. http://dx.doi.org/10.1071/9780643090071.

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This authoritative catalogue will greatly assist readers in finding the correct taxonomic name for any given family, genus or species within each of the six arachnid orders treated. It contains a valuable summary of bibliographic information, enabling readers to access the worldwide literature for these smaller orders. The catalogue presents full bibliographic data on each of the taxa named thus far, treating over 1600 species. It contains the most current classification system for each group, some of which have not been catalogued on a world scale for over 70 years. A summary of taxonomic changes is included. This quality reference will be of immense value to arachnologists, systematists, taxonomists, ecologists and biodiversity professionals, especially those interested in tropical rainforest communities.

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32

Stoddard, Frederick J., and Robert L. Sheridan. Wound Healing and Depression. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603342.003.0009.

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Depression and wound healing are bidirectional processes for adults and children consistent with the conception of depression as systemic. This systemic interaction is similar to the “bidirectional impact of mood disorder on risk for development, progression, treatment, and outcomes of medical illness” generally. And, evidence is growing that the bidirectional impact of mood disorder may be true for injuries and for trauma surgery. Animal models have provided some support that treatment of depression may improve wound healing. An established biological model for a mechanism delaying wound healing is increased cortisol secretion secondary to depression and/or stress, and impaired immune response, in addition or together with the other factors such as genetic or epigenetic risk for depression. Cellular models relate both to wound healing and to depression include cytokines, the inflammatory response (Miller et al, 2008), and cellular aging (Telgenhoff and Shroot, 2005) reflected in shorter leukocyte telomere length (LTL) (Verhoeven et al, 2016). Another model of stress impacting wound healing investigated genetic correlates—immediate early gene expression or IEG from the medial prefrontal cortex, and locomotion, in isolation-reared juvenile rats. Levine et al (2008) compared isolation reared to group reared samples, and found that, immediate gene expression in the medial prefrontal cortex (mPFC) was reduced, and behavioral hyperactivity increased, in juvenile rats with 20% burn injuries. Wound healing in the isolation reared rats was significantly impaired. They concluded that these results provide candidates for behavioral biomarkers of isolation rearing during physical injury, i.e. reduced immediate mPFC gene expression and hyperactivity. They suggested that a biomarker such as IEGs might aid in demarcating patients with resilient and adaptive responses to physical illness from those with maladaptive responses

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33

Methods in Neurosciences: Neuropeptide Analogs, Conjugates, and Fragments (Methods in Neurosciences). Academic Press, 1993.

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