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Books on the topic 'Immune response genes'

Author: Grafiati

Published: 4 June 2021

Last updated: 28 July 2024

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1

Mak, Tak W. Handbook of immune response genes. Plenum Press, 1998.

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2

Marc, Feldmann, and McMichael Andrew J, eds. Regulation of immune gene expression. Humana Press, 1986.

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3

J, Kay, ed. Genes and proteins in immunity. Biochemical Society, 1986.

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4

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. Liss, 1988.

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5

Ottenhoff, Thomas Henricus Maria. HLA class II immune response genes in leprosy: Studies on the recognition of Mycobacterium leprae antigens and class II molecules by cloned human T cells. [s.n.], 1986.

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6

Derek, Wakelin, and Blackwell J. M, eds. Genetics of resistance to bacterial and parasitic infection. Taylor & Francis, 1988.

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7

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

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8

Mak, Tak W., and John J. L. Simard. Handbook of Immune Response Genes. Springer, 2013.

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9

Feldmann, Marc, and Andrew McMichael. Regulation of Immune Gene Expression. Humana Press, 2012.

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10

Feldmann, Marc, and Andrew McMichael. Regulation of Immune Gene Expression. Humana Press, 2012.

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11

Molecular basis of the immune response. New York Academy of Sciences, 1988.

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12

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

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13

Cunningham, Alastair J., and Eli Sercarz. Strategies of Immune Regulation. Elsevier Science & Technology Books, 2013.

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14

Genes and proteinsin immunity. Biochemical Society, 1986.

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15

Sehgal, Pravinkumar B., and Gerd Grieninger. Regulation of the Acute Phase and Immune Responses: Interleukin-6 (Annals of the New York Academy of Sciences, Vol. 557). New York Academy of Sciences, 1989.

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16

Aptsiauri, Natalia, Angel Miguel Garcia-Lora, and Teresa Cabrera. MHC Class I Antigens In Malignant Cells: Immune Escape And Response To Immunotherapy. Springer, 2013.

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17

Aptsiauri, Natalia, Angel Miguel Garcia-Lora, and Teresa Cabrera. MHC Class I Antigens in Malignant Cells: Immune Escape and Response to Immunotherapy. Springer, 2013.

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18

Regulatory idiotopes. Wiley, 1987.

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19

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

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20

Parkes, Joanna E., Simon Rothwell, and Janine A. Lamb. Aetiology and pathogenesis. Edited by Hector Chinoy and Robert Cooper. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198754121.003.0003.

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The aetiology and pathogenesis of idiopathic inflammatory myopathies (IIM) is poorly understood; IIM are thought to result from exposure to environmental factors in genetically susceptible individuals. Both innate and adaptive immune responses are involved in IIM, and there is increasing evidence that non-inflammatory mechanisms play an important role in disease pathology. Several environmental risk factors, including infectious agents, ultraviolet radiation, cigarette smoking, and exposure to statins, have been implicated. Genetic studies have identified the major histocompatibility complex a

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21

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 ph

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22

Winchester, Robert, Darren D. O’Rielly, and Proton Rahman. Genetics of psoriatic arthritis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198737582.003.0006.

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The psoriatic phenotype is clinically heterogeneous with psoriatic arthritis (PsA) itself being heterogeneous. Studies have consistently demonstrated that PsA has a strong genetic component and disease pathogenesis encompasses a complex interplay between genetic, immunological, and environmental factors. In this chapter, we will review the genetics of PsA including the major histocompatibility complex (MHC) region and non-MHC loci. We will detail how susceptibility genes can be grouped into barrier integrity, innate immune response, and adaptive immune response (particularly Th-17 lymphocyte s

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23

Somatic Diversification of Immune Responses (Current Topics in Microbiology and Immunology). Springer-Verlag Telos, 1998.

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24

Geri, Guillaume, and Jean-Paul Mira. Host–pathogen interactions in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0306.

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Infection by a pathogenic micro-organism triggers a coordinated activation of both innate and adaptive immune responses. The innate immune response quickly triggers an antimicrobial response that will initiate development of a pathogen-specific, long-lasting adaptive immune response. Accurate recognition of microbial-associated molecular patterns by pattern-recognition receptors (PRRs) is the cornerstone of this immediate response. Most studied PRRs are Toll-like receptors (TLRs) and their kinase signalling cascades that activate nuclear transcription factors, and induce gene expression and cy

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25

de Vlam, Kurt. Overview of psoriatic arthritis pathogenesis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198737582.003.0004.

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Psoriatic arthritis (PsA) is a chronic inflammatory arthritis occurring in patients with psoriasis. Some consider it as part of the heterogeneous group of diseases unified in the concept of spondyloarthritis (SpA). At least some subtypes, such as the oligoarticular and axial subtypes, can be classified as SpA. The aetiology and pathogenesis are poorly understood. An enthesitis-based model was proposed to unify skin and joint manifestation and to differentiate PsA from other rheumatic diseases such as rheumatoid arthritis and osteoarthritis. The development of PsA results from the interplay of

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26

Kishore, Uday. Target Pattern Recognition in Innate Immunity. Springer London, Limited, 2010.

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27

(Editor), Ward E. Bullock, Nabil Hanna (Editor), and Toby K. Eisenstein (Editor), eds. Host Defenses and Immunomodulation to Intracellular Pathogens (Advances in Experimental Medicine & Biology). Springer, 1988.

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28

Odds, Frank C. Pathogenesis 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/9780198755388.003.0008.

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The pathogenesis of fungal disease involves an interplay between fungal virulence factors and host immune responses. Most fungal pathogens are opportunists that preferentially invade hosts with immune defects, but the fact that relative pathogenicity varies between fungal species (and even between different strains within a species) is evidence that fungi have evolved multiple, different molecular virulence factors. Experiments in which genes encoding putative virulence attributes are specifically disrupted and the resulting mutants are tested for virulence in a range of vertebrate and inverte

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29

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 therap

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30

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 heal

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31

Halliday, Catriona L., and Sarah E. Kidd. Cryptococcus species. 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/9780198755388.003.0012.

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Cryptococcus neoformans and Cryptococcus gattii are the principal pathogenic species within the genus Cryptococcus and the causative agents of cryptococcosis. Although rare, the incidence of infection due to other Cryptococcus species previously regarded as saprophytes, has increased over the last 40 years. Irrespective of the infecting species, infections are acquired following inhalation from the environment, causing localised or disseminated disease. The severity of disease is dependent on the organism’s virulence factors and the host’s immune response, and the clinical manifestations are i

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32

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

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33

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 diseas

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34

Dalbeth, Nicola. Clinical features of gout. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198748311.003.0005.

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About 60% of the variance in serum urate levels can be explained by inherited genetic factors, but the extent of the contribution of genetic factors to gout in the presence of hyperuricaemia is not known. Genome-wide association studies in Europeans have identified 28 loci controlling serum urate levels, although the molecular basis of the majority of these genetic associations is currently unknown. The SLC2A9 and ABCG2 renal and gut uric acid transporters have very strong effects on urate levels and the risk of gout. Other uric acid transporters (e.g. SLC22A11/OAT478, SLC22A12/URAT1) and a gl

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35

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

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36

Jex, Aaron R., Rachel M. Chalmers, Huw V. Smith, Giovanni Widmer, Vincent McDonald, and Robin B. Gasser. Cryptosporidiosis. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0053.

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Cryptosporidium species represent a genus of parasitic protozoa (Apicomplexa) that are transmitted via the faecal-oral route and commonly infect the epithelial tissues of the gastric or intestinal (or sometimes the respiratory) tract of many vertebrates, including humans. Infection occurs following the ingestion of viable and resistant oocysts, through direct host-to-host contact or in contaminated food, drinking or recreational water. Infection can be transmitted via anthroponotic (human-to-human, human-to-animal) or zoonotic (animal-to-human or animal-to-animal) pathways, depending upon the

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37

Cui, Zhao, Neil Turner, and Ming-hui Zhao. Alport post-transplant antiglomerular basement membrane disease. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0075.

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Alport antiglomerular basement membrane (anti-GBM) disease is a rare example of disease caused by allo-sensitization after renal transplantation, first described in 1992. Because the recipient lacks a specific glomerular basement membrane (GBM) protein, they can become sensitized to the normal molecule present in the GBM of the donor kidney. The disease is restricted to the allograft. Interestingly severe disease arises from this only arises rarely, certainly less than 1 in 20, probably closer to 1 in 50. It characteristically causes late graft loss in a first transplant with accelerated tempo

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38

Simpson, A., E. Aarons, and R. Hewson. Marburg and Ebola viruses. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0038.

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Infection with Marburg and Ebola viruses cause haemorrhagic fevers that are characterized by organ malfunction, bleeding complications, and high mortality. The viruses are members of the family Filoviridae, a group of membrane-enveloped filamentous RNA viruses. Five distinct species of the genus Ebolavirus have been reported; the genus Marburgvirus contains only one species. Both Marburg and Ebola virus diseases are zoonotic infections whose primary hosts are thought to be bats. The initial human infection is acquired from wildlife and subsequent person-to-person spread propagates the outbreak

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