Books: 'Immune response genes'

1

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

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2

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

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3

J, Kay, ed. Genes and proteins in immunity. London: 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. New York: 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.l.]: [s.n.], 1986.

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6

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

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7

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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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, N.Y: 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. London: 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. New York: 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 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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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 as the most strongly associated region, while recent large scale genome-wide studies have implicated genes that commonly regulate the adaptive immune response, which overlap with other seropositive autoimmune diseases. Integrating data across these various fields should facilitate refined models of disease pathogenesis.

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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 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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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 signalling). We will articulate how these studies strongly support PsA as genetically different from PsV and that the genetic heterogeneity is likely attributed to different HLA susceptibility alleles within the MHC region that an individual carries. Furthermore, we will highlight new emerging technologies, in particular, next-generation sequencing, which may lead to new genetic discoveries in PsA.

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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 cytokine production. Deficiencies or genetic variability in these different signalling pathways may lead to recurrent pyogenic infections and severe invasive diseases. After initial contact between the host and pathogen, numerous factors mediate the inflammatory response, as pro-inflammatory cytokines and chemokines. Apart from host genetic variability, pathogen diversity also influences the phenotypic features of various infectious diseases. Genomic analysis may assist in the development of targeted therapies or new therapeutic strategies based on both patient and microorganism genotype.

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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 genes, the immune response, and interaction with environmental factors. The fact that more than 80% of patients with PsA have precedent or simultaneous psoriasis suggests that the skin disease is almost a ‘condicio sine qua non’ for the development of PsA.

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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 invertebrate hosts have identified or confirmed many gene products as significant for the pathogenesis of various types of fungal disease. These include factors determining fungal shape in vivo, biofilm formation, and a plethora of surface components, including adhesins and hydrolytic enzymes. This chapter provides an overview of fungal virulence attributes.

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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 therapy are being evaluated with the aim of achieving HIV-1 control without antiretroviral therapy, if not viral eradication.

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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 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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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 indistinguishable. Accurate identification of the pathogenic species relies on rDNA sequencing

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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 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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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 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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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 glycolysis gene (GCKR) are associated with urate levels. Environmental exposures such as sugar-sweetened beverages and alcohol interact with urate-associated genetic variants in an unpredictable fashion. Very little is known about the genetic control of gout in the presence of hyperuricaemia, formation of monosodium urate crystals, and the immune response.

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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 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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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 species of Cryptosporidium. Although infection can be asymptomatic, common symptoms of disease (cryptosporidiosis) include diarrhoea, colic (abdominal pain), nausea or vomiting, dehydration and/or fever. In humans, cryptosporidial infection in immunocompetent patients is usually short-lived (days to weeks) and eliminated following the stimulation of an effective immune response. However, infection in immunodeficient individuals (e.g., those with HIV/AIDS) can be chronic and fatal (in the absence of immunotherapy), as there are few effective anti-cryptosporidial drugs and no vaccines available. The present chapter provides an account of the history, taxonomy and biology, genomics and genetics of Cryptosporidium, the epidemiology, pathogenesis, treatment and control of cryptosporidiosis and the advances in tools for the identification and characterisation of Cryptosporidium species and the diagnosis of cryptosporidiosis.

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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 in later allografts, and in its most extreme form recurs within days. However, inexplicably some subsequent transplants do not provoke aggressive recurrence. Treatment of the most aggressive disease is difficult and in most cases has been ultimately unsuccessful. Lower levels of immune response, marked by linear binding of immunoglobulin-G to GBM without glomerular disease, are not uncommon in Alport patients after transplantation and should not lead to altered treatment. Immunoassays for anti-GBM antibodies can be misleading as in most cases the target of antibodies is the α‎‎‎5 chain of type IV collagen, rather than the α‎‎‎3 chain which is the target in spontaneous anti-GBM disease. Overall the outcome of transplantation in Alport syndrome is better than average. This complication is more likely in patients with partial or total gene deletion rather than point mutations, but no other predictive features have been identified.

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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 until it is brought under control. Ebola and Marburg viruses are classified as hazard or risk group 4 pathogens because of the very high case fatality rates observed for Ebola and Marburg virus diseases, the frequency of person-to-person transmission and community spread, and the lack of an approved vaccine or antiviral therapy. This mandates that infectious materials are handled and studied in maximum containment laboratory facilities. Epidemics have occurred sporadically since the discovery of Marburg in 1967 and Ebola virus in 1976. While some of these outbreaks have been relatively large, infecting a few hundreds of individuals, they have generally occurred in rural settings and have been controlled relatively easily. However, the 2013–2016 epidemic of Ebola virus disease in West Africa was different, representing the first emergence of the Zaire species of Ebola in a high-density urban location. Consequently, this has been the largest recorded filovirus outbreak in both the number of people infected and the range of geographical spread. Many of the reported and confirmed cases were among people living in high-density and impoverished urban environments. The chapter summarizes the most up-to-date taxonomic status of the family Filoviridae. It focuses on Marburg and Ebola viruses in a historical context, culminating in the 2013–2016 outbreak of Ebola virus in West Africa. Virus biology of the most well-studied member is described, with details of the viral genome and the protein machinery necessary to propagate viruses at the molecular and cellular level. This information is used to build a wider-scale virus–host perspective with detail on the pathology and pathogenesis of Ebola virus disease. The consequences of cell infection are examined, together with our current understanding of the immune response to Ebola virus, leading to a broader description of the clinical features of disease. The chapter closes by drawing information together in a section on diagnosis, ecology, prevention, and control.

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Books on the topic 'Immune response genes'

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