Academic literature on the topic 'Immunogenetics (incl. Genetic Immunology)'
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Journal articles on the topic "Immunogenetics (incl. Genetic Immunology)"
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Breaux, Breanna, Ashley Heard-Ganir, Leo Sena, Margaret Hunter, Robert Bonde, and Michael Criscitiello. "Understanding manatee immunogenetics and the implications for conservation (VET1P.1121)." Journal of Immunology 194, no. 1_Supplement (May 1, 2015): 146.9. http://dx.doi.org/10.4049/jimmunol.194.supp.146.9.
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Abstract The completion of the genome draft of the Florida manatee (Trichechus manatus latirostris) in 2012 made immunogenetic exploration of the Sirenia order more feasible. The endangered manatees are sentinel species for coastal ecosystems and their evolutionary origins are complex. It is believed that they evolved from a wading terrestrial mammal that became fully aquatic, which suggests distinctive adaptations for transitioning to a new environment. Discovering the genetic details of their immune system will help understand manatee evolution and allow species-specific diagnostic tools to be developed. Due to bottleneck signatures at other loci, the genetic diversity of the major histocompatibility complex (MHC) is expected to be low. This could pose problems for conservation efforts because low diversity can increase the chance of extirpation. The primary focus of this project is to determine the immune robustness of manatees by looking at their antibody repertoire and MHC polymorphism. Two species will be compared: the West Indian manatee (T. manatus) and the Amazonian manatee (T. inunguis). Using next generation sequencing, we will robustly sample the IgH and IgL rearrangements contributing to the antibody repertoire, and identify dominant MHC alleles and estimate their frequencies. The allelic distribution between the species could reveal clues to their evolutionary relationship and aid conservation efforts to help this species become more stable in their environment.
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Niebergall, Emily R., Emily A. Beck, Susan Bassham, and William A. Cresko. "Advancing threespine stickleback as an outbred immunogenetics model by pinpointing the onset of adaptive immunity." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 53.25. http://dx.doi.org/10.4049/jimmunol.202.supp.53.25.
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Abstract The development of an outbred immunogenetics model system is needed to understand how genetic variation impacts phenotypic variation of disease states in humans. Threespine stickleback fish (Gasterosteus aculeatus) provide just such a model. Stickleback are genetically tractable laboratory organisms with a well-annotated genome, but with lines drawn from populations inhabiting vastly different habitats. Individuals from different populations show high levels of genetic variation. The onset of the adaptive immune system is currently unknown in stickleback, a significant hindrance in studies of immunodeficiency diseases. To characterize the early development of adaptive immunity, we will analyze the expression of known early indicators of adaptive immunity maturation. These include recombination activating genes, rag1 and rag2, which are essential to the maturation of T and B lymphocytes, and T cell receptor genes, tcr-β and tcr-γ, which are expressed in mature T lymphocytes. To analyze the expression of rag1, rag2, tcr-β, and tcr-γ, we will perform whole mount in situ hybridization throughout a developmental time series to detect when and where the genes are first expressed, with special focus on the head kidney and the thymus, followed by qPCR to quantify the expression of the early adaptive immunity genes. Knowing when adaptive immunity onset occurs in threespine stickleback advances threespine stickleback as an outbred disease model in immunogenetics studies, allowing manipulative studies of immunological disease phenotypes in the context of genetic variation.
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Criscitiello, Michael F. "Activation Induced Cytidine Deaminase and the Evolution of Antigen Receptor Immunogenetics." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 92.10. http://dx.doi.org/10.4049/jimmunol.204.supp.92.10.
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Abstract All jawed vertebrates share fundamental components of the adaptive immune system. Cartilaginous fish are the most divergent jawed vertebrate group relative to mammals and use a major histocompatibility complex, B cells, and T cells. RAG mediates the rearrangement of gene segments to create both B and T cell receptors. B cell receptors further undergo diversification after antigen exposure when activated B cells extensively alter their rearranged genes to enhance affinity to antigen. This receptor modification is mediated by the enzyme activation-induced cytidine deaminase (AID). Remarkably, AID also catalyzes receptor modifications in alpha chain of TCR within shark thymus. Thus, the ancestor to modern vertebrates may have used an AID-like enzyme for lymphocyte receptor development, a mechanism lost in later vertebrates because of its potential for breaking down self-tolerance in mature lymphocytes. At the other end of the vertebrate tree, the repertoire of Bos taurus antibodies is characterized by a subset of heavy chains with variable domains VH encoding ultralong complementarity determining region CDR3. These ultralong CDR3 range from forty to over seventy amino acids in length and form a unique beta-ribbon “stalk” and disulfide bonded “knob”. Deep sequence analysis of the B. taurus heavy chain repertoire unveiled ultralong CDR3s were products of rearrangement between the longest VH and DH segments, IGHV1-1 and DH8. Both germline and somatic genetic factors and processes appear to be involved in diversification of this structurally unusual bovine ultralong CDR3 repertoire. These unheralded uses of AID will be discussed in the broader context of immunogenetics evolution.
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Gerussi, Alessio, Ambra Natalini, Fabrizio Antonangeli, Clara Mancuso, Elisa Agostinetto, Donatella Barisani, Francesca Di Rosa, Raul Andrade, and Pietro Invernizzi. "Immune-Mediated Drug-Induced Liver Injury: Immunogenetics and Experimental Models." International Journal of Molecular Sciences 22, no. 9 (April 27, 2021): 4557. http://dx.doi.org/10.3390/ijms22094557.
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Drug-induced liver injury (DILI) is a challenging clinical event in medicine, particularly because of its ability to present with a variety of phenotypes including that of autoimmune hepatitis or other immune mediated liver injuries. Limited diagnostic and therapeutic tools are available, mostly because its pathogenesis has remained poorly understood for decades. The recent scientific and technological advancements in genomics and immunology are paving the way for a better understanding of the molecular aspects of DILI. This review provides an updated overview of the genetic predisposition and immunological mechanisms behind the pathogenesis of DILI and presents the state-of-the-art experimental models to study DILI at the pre-clinical level.
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Adamczuk, Marcin, Piotr Zaleski, Lukasz Dziewit, Renata Wolinowska, Marta Nieckarz, Pawel Wawrzyniak, Piotr Kieryl, Andrzej Plucienniczak, and Dariusz Bartosik. "Diversity and Global Distribution of IncL/M Plasmids Enabling Horizontal Dissemination ofβ-Lactam Resistance Genes among the Enterobacteriaceae." BioMed Research International 2015 (2015): 1–12. http://dx.doi.org/10.1155/2015/414681.
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Antibiotic resistance determinants are frequently associated with plasmids and other mobile genetic elements, which simplifies their horizontal transmission. Several groups of plasmids (including replicons of the IncL/M incompatibility group) were found to play an important role in the dissemination of resistance genes encodingβ-lactamases. The IncL/M plasmids are large, broad host range, and self-transmissible replicons. We have identified and characterized two novel members of this group: pARM26 (isolated from bacteria inhabiting activated sludge from a wastewater treatment plant) and pIGT15 (originating from a clinical strain ofEscherichia coli). This instigated a detailed comparative analysis of all available sequences of IncL/M plasmids encodingβ-lactamases. The core genome of these plasmids is comprised of 20 genes with conserved synteny. Phylogenetic analyses of these core genes allowed clustering of the plasmids into four separate groups, which reflect their antibiotic resistance profiles. Examination of the biogeography of the IncL/M plasmids revealed that they are most frequently found in bacteria of the family Enterobacteriaceae originating from the Mediterranean region and Western Europe and that they are able to persist in various ecological niches even in the absence of direct antibiotic selection pressure.
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Eden, Peter A., Gregory J. Christianson, Pierre Fontaine, Peter J. Wettstein, Claude Perreault, and Derry C. Roopenian. "Biochemical and Immunogenetic Analysis of an Immunodominant Peptide (B6dom1) Encoded by the Classical H7 Minor Histocompatibility Locus." Journal of Immunology 162, no. 8 (April 15, 1999): 4502–10. http://dx.doi.org/10.4049/jimmunol.162.8.4502.
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Abstract Of the many minor histocompatibility (H) Ags that have been detected in mice, the ability to induce graft vs host disease (GVHD) after bone marrow transplantation is restricted to a limited number of immunodominant Ags. One such murine Ag, B6dom1, is presented by the H2-Db MHC class I molecule. We present biochemical evidence that the natural B6dom1 peptide is indistinguishable from AAPDNRETF, and we show that this peptide can be isolated from a wide array of tissues, with highest levels from the lymphoid organs and lung. Moreover, we employ a novel, somatic cell selection technique involving CTL-mediated immunoselection coupled with classical genetics, to show that B6dom1 is encoded by the H7 minor H locus originally discovered ∼40 years ago. These studies provide a molecular genetic framework for understanding B6dom1, and exemplify the fact that mouse minor H loci that encode immunodominant CTL epitopes can correspond to classical H loci originally identified by their ability to confer strong resistance to tumor transplantation. Additionally, these studies demonstrate the utility of somatic cell selection approaches toward resolving H Ag immunogenetics.
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Khatri, Indu, Magdalena A. Berkowska, Erik B. van den Akker, Cristina Teodosio, Marcel J. T. Reinders, and Jacques J. M. van Dongen. "Population matched (pm) germline allelic variants of immunoglobulin (IG) loci: Relevance in infectious diseases and vaccination studies in human populations." Genes & Immunity 22, no. 3 (June 12, 2021): 172–86. http://dx.doi.org/10.1038/s41435-021-00143-7.
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AbstractImmunoglobulin (IG) loci harbor inter-individual allelic variants in many different germline IG variable, diversity and joining genes of the IG heavy (IGH), kappa (IGK) and lambda (IGL) loci, which together form the genetic basis of the highly diverse antigen-specific B-cell receptors. These allelic variants can be shared between or be specific to human populations. The current immunogenetics resources gather the germline alleles, however, lack the population specificity of the alleles which poses limitations for disease-association studies related to immune responses in different human populations. Therefore, we systematically identified germline alleles from 26 different human populations around the world, profiled by “1000 Genomes” data. We identified 409 IGHV, 179 IGKV, and 199 IGLV germline alleles supported by at least seven haplotypes. The diversity of germline alleles is the highest in Africans. Remarkably, the variants in the identified novel alleles show strikingly conserved patterns, the same as found in other IG databases, suggesting over-time evolutionary selection processes. We could relate the genetic variants to population-specific immune responses, e.g. IGHV1-69 for flu in Africans. The population matched IG (pmIG) resource will enhance our understanding of the SHM-related B-cell receptor selection processes in (infectious) diseases and vaccination within and between different human populations.
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Quigley, Bonnie L., Galit Tzipori, Karen Nilsson, and Peter Timms. "High-throughput immunogenetic typing of koalas suggests possible link between MHC alleles and cancers." Immunogenetics 72, no. 9-10 (October 20, 2020): 499–506. http://dx.doi.org/10.1007/s00251-020-01181-7.
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AbstractCharacterizing the allelic diversity within major histocompatibility complex (MHC) genes is an important way of determining the potential genetic resilience of a population to infectious and ecological pressures. For the koala (Phascolarctos cinereus), endemic diseases, anthropogenic factors and climate change are all placing increased pressure on this vulnerable marsupial. To increase the ability of researchers to study MHC genetics in koalas, this study developed and tested a high-throughput immunogenetic profiling methodology for targeting MHC class I UA and UC genes and MHC class II DAB, DBB, DCB and DMB genes in a population of 82 captive koalas. This approach was validated by comparing the determined allelic profiles from 36 koala family units (18 dam-sire-joey units and 18 parent-joey pairs), finding 96% overall congruence within family profiles. Cancers are a significant cause of morbidity in koalas and the risk factors remain undetermined. Our analysis of this captive population revealed several novel MHC alleles, including a potential link between the DBB*03 allele and a risk of developing cancer. This method offers a reliable, high-throughput protocol for expanded study into koala immunogenetics.
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Sika-Paotonu, Dianne, Pedro Azevedo, Allamanda Faatoese, Helen Wihongi, Hiueni Nuku, Maui Hudson, Palatasa Havea, Tom Parks, Tony Merriman, and Diana Lennon. "Culturally appropriate advisory and governance oversight for the study of rheumatic fever and rheumatic heart disease in New Zealand." Journal of Immunology 198, no. 1_Supplement (May 1, 2017): 125.30. http://dx.doi.org/10.4049/jimmunol.198.supp.125.30.
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Abstract Acute rheumatic fever (ARF) is an autoimmune condition caused by untreated Group A Streptococcal (GAS) infection of the upper respiratory tract (and possibly skin). Multiple or severe attacks of ARF can cause cardiac damage, known as Rheumatic Heart Disease (RHD). RHD remains a significant cause of morbidity and mortality is rare in developed countries. In New Zealand, the disease burden of ARF and RHD amongst Indigenous Maori and Pasifika communities is one of the highest in the world, usually affecting children and young adults. Previous work carried out in New Zealand sought to explore the immunogenetics of ARF and RHD and involved candidate gene analysis techniques utilizing samples from individuals diagnosed with RHD where a functional variant in the gene encoding the interleukin IL-6 cytokine known as IL-6 rs1800797 was found to be significantly associated with RHD. Current work seeks to explore the genetic susceptibility to ARF/RHD in greater depth using more advanced genome-wide technology. An international genome wide association study (GWAS) is currently underway to further understand the genetics of ARF/RHD using data obtained from global sources. To undertake the proposed GWAS work and amend the original New Zealand study, an Advisory team comprised of Pasifika and Māori representatives comprised of community leaders, researchers, scientists, and academics is providing the appropriate governance, cultural support and guidance essential for the project work.
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Szczawinska-Poplonyk, Aleksandra, Kinga Begier, Alicja Dorota, Monika Dabrowska, Dominika Galecka, Kamila Wawrzeniak, and Kamil Wroblewski. "Syndromic immunodeficiencies: a pediatrician’s perspective on selected diseases." Allergologia et Immunopathologia 49, no. 4 (July 1, 2021): 117–36. http://dx.doi.org/10.15586/aei.v49i4.200.
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Background: Syndromic immunodeficiencies are a genetically and pathophysiologically heterogeneous group of inborn errors of immunity. These are characterized by multiple extra immune clinical symptoms and a wide range of immunological phenotypes with increased susceptibility to infections, autoimmune phenomena, immune dysregulation, organ-specificpathology, and malignancy.Objective: To increase the pediatricians’ awareness of this multifaceted group of primary immunodeficiencies in children.Methods: A comprehensive review of genetic background and clinical symptomatology of syndromic immunodeficiencies as well as current diagnostic approach and treatment modalities.Results: From the pediatrician’s perspective, an early-life diagnosis of syndromic immunodeficiencies, which is frequently indispensable for successful life-saving immunocorrection, poses a diagnostic challenge. Increased pediatricians’ awareness to recognize signs and symptoms of these diseases in affected children is of paramount importance. Current advances in molecular biotechnology and immunogenetics, resulting in the implementation of newborn screening and new-generation sequencing, provide informative tools for definitive diagnosis and, in many new disease entities, for their definition and genotype–phenotype delineation and correlation.Conclusions: A broad spectrum of clinical phenotypes in children with syndromic primary immunodeficiencies requires pediatrician’s special attention, that is, individualized multidisciplinary approach under the supervision of a clinical immunologist.
Dissertations / Theses on the topic "Immunogenetics (incl. Genetic Immunology)"
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Yu, Chack-yung. "The gene structure and the polymorphism of the human complement component C4." Thesis, University of Oxford, 1987. http://ora.ox.ac.uk/objects/uuid:5a8473fb-01c1-43a1-961b-6c23f41c93f4.
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1. The DNA sequence of the human complement C4A gene from a cosmid clone Cos 3A3 was determined and the complete exon-intron structure elucidated. The 5' flanking region of the C4 gene contains three TATA sequences and a transcriptional enhancer core sequence, which are >200 nucleotides (nt) and 60-70 nt upstream from the CAP site, respectively. The gene consists of 42 exons coding for a precursor protein of 1745 residues. The first exon codes for a 51 nt 5' untranslated sequence, a leader peptide of 19 residues, and the N-terminus of the β chain. The β-α and the α-γ chain junctions are encoded by exons 17 and 34, respectively. The anaphylatoxin C4a and the thiolester site are encoded by phase 1-1 symmetrical exons. Most of the amino acids encoded at the splice junctions are polar or charged. Between exons 10 and 11 is a 6-7 kb intron that is flanked by direct long terminal repeats and may be absent in some C4 genes located at the second C4 locus. The last exon codes for the C-terminus of the γ chain and a 140 bp 3' untranslated sequence. The intergenic region between the C4 gene and its neighbouring 21-hydroxylase (210Hase) gene is ~3028 bp. 2. Eighteen polymorphic amino acids on C4 have been identified through genomic DNA, cDNA and protein sequencing. Fourteen of them are located on the* chain (C4a: 2 changes; C4d: 12 changes). The rest are scattered on the β and the γ chains. There are potential size variations by one residue on the β chain, and by a tripeptide that contains a sulphation site on the α chain. 3. Four common and rare C4 alleles have been cloned from individuals whose C4 proteins were chemically and serologically characterised. Analysis of the sequences at the C4d regions has allowed the identification of the C4A/C4B isotypic residues at positions 1101-6: C4A has the sequence PCPVLD, while C4B has the sequence LSPVIH. Presumably these isotypic residues are the cause of the class-specific, differential chemical reactivates. Moreover, the probable locations for the two Eodgers (Kg) and the six Chido (Ch) antigenic determinants were deduced. The C4B isotypic residues may be involved in the expression of the Ch2 and the Ch4 epitopes, while the C4A isotypic residues may not be related to either of the Eg determinants. 4. Definitive restriction fragment length polymorphisms (RFLPs) representing the exact locations responsible for the isotypicity between C4A and C4B, and for their generally associated Rg1 and Ch1 antigenic determinants, have been designed. In combination with the Taq I polymorphic patterns specific for the C4 and for the 210Hase gene loci, it has been shown that the null allele of the HLA haplotype B44 DR6 C4A 3 C4B QO is not a C4B allele, but probably encodes another C4A 3 allotype at the second C4 locus.
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Brown, Michael Paul. "Investigation of the therapeutic potential of transgenic CD40 ligand expression." 2007. http://hdl.handle.net/2440/50727.
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The CD40 ligand (CD40L) molecule is central to innate and adaptive immunity. CD40L expression is very tightly regulated whereas its CD40 receptor is constitutively expressed by many different cell types. CD40L is expressed transiently on helper T cells (Th) only after activation by specific immune recognition molecules carried by professional antigen presenting cells, in particular, dendritic cells (DC). CD40L subsequently binds to CD40 on DC to enable full Th activation. CD40 ligated DC produce interleukin-12 (IL-12) and contribute both to the development of IFNγ-secreting natural killer cells, a vital component of innate immunity, and of IFNγ-secreting type 1 Th (Th1) cells. CD40 ligated DC also contribute to the development of IL-4- and IL-10-secreting Th2 cells. CD40L on Th cells also binds CD40 on macrophages to enhance their cytotoxic functions. CD40L-expressing Th cells provide the ‘help’ pivotally required to activate other components of adaptive immunity responsible both for clearing invading pathogens and generating the memory cells required to prevent re-infection. Th-supplied CD40L binds (i) B cell CD40 to switch production of antibodies to more potent effector molecules that have higher avidity for antigen, and (ii) DC CD40 to prime then expand antigen-specific cytotoxic T lymphocytes (CTL). Activated NK cells and CTL are required both to eradicate malignant cells and cells infected with viruses or other intracellular pathogens. Genetic CD40L deficiency causes the very rare HyperIgM Syndrome Type 1 (HIGM1), which is realistically modelled by genetically engineered CD40L-deficient mice. Neither CD40L-deficient patients nor mice make effective antibodies or mount cellular immune responses that would defend them against intracellular pathogens such as parasites. Consequently, the only potentially curative therapy is allogeneic stem cell transplantation or CD40L gene replacement. Here, we used a retroviral vector, which constitutively expressed CD40L, to genetically modify CD40L-deficient bone marrow cells, which were used to reconstitute partially the immunity of CD40L-deficient mice. The crucial importance of tight regulation of CD40L expression was revealed when these mice later developed lethal thymic T cell malignancy. Growing tumours escape immune vigilance by genetic alterations that reduce their sensitivity to IFNγ. Using murine tumour models, we incorporated transgenic CD40L expression in therapeutic tumour vaccines to show that CD40L gene transfer augmented the immunogenicity of the host’s tumour thus reducing its tumorigenicity. We translated this finding clinically to safety and immunogenicity testing of a transgenic CD40L- and IL-2- expressing leukaemia vaccine. Finally, the common viral respiratory pathogen, respiratory syncytial virus (RSV) mainly infects young infants and the elderly to cause potentially lethal pneumonia. Both groups have reduced cellular and humoral immunity, which predisposes them to re-infection with RSV. Using a murine model, we showed first that simultaneous adenoviral expression of CD40L augmented primary RSV-specific Th1 responses that were associated with accelerated pulmonary viral clearance. Second, we showed that expression of CD40L in RSV-F and RSV-G subunit DNA vaccines elevated antibody and cellular immune responses to RSV challenge four and eight months after the initial immunisation. These results demonstrate the potent ability of CD40L gene transfer to solve the absolute immune deficiency caused by genetic lesions of CD40L. However, physiological regulation of the transgene is required to prevent serious adverse consequences. In contrast, no adverse effects were observed after transgenic CD40L expression was used to overcome relative immune deficiencies imposed by malignancy and RSV infection.http://proxy.library.adelaide.edu.au/login?url= http://library.adelaide.edu.au/cgi-bin/Pwebrecon.cgi?BBID=1298200
Thesis (Ph.D.) - University of Adelaide, School of Medicine, 2007
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Brown, Michael Paul. "Investigation of the therapeutic potential of transgenic CD40 ligand expression." Thesis, 2007. http://hdl.handle.net/2440/50727.
Full textAbstract:
The CD40 ligand (CD40L) molecule is central to innate and adaptive immunity. CD40L expression is very tightly regulated whereas its CD40 receptor is constitutively expressed by many different cell types. CD40L is expressed transiently on helper T cells (Th) only after activation by specific immune recognition molecules carried by professional antigen presenting cells, in particular, dendritic cells (DC). CD40L subsequently binds to CD40 on DC to enable full Th activation. CD40 ligated DC produce interleukin-12 (IL-12) and contribute both to the development of IFNγ-secreting natural killer cells, a vital component of innate immunity, and of IFNγ-secreting type 1 Th (Th1) cells. CD40 ligated DC also contribute to the development of IL-4- and IL-10-secreting Th2 cells. CD40L on Th cells also binds CD40 on macrophages to enhance their cytotoxic functions. CD40L-expressing Th cells provide the ‘help’ pivotally required to activate other components of adaptive immunity responsible both for clearing invading pathogens and generating the memory cells required to prevent re-infection. Th-supplied CD40L binds (i) B cell CD40 to switch production of antibodies to more potent effector molecules that have higher avidity for antigen, and (ii) DC CD40 to prime then expand antigen-specific cytotoxic T lymphocytes (CTL). Activated NK cells and CTL are required both to eradicate malignant cells and cells infected with viruses or other intracellular pathogens.
Genetic CD40L deficiency causes the very rare HyperIgM Syndrome Type 1 (HIGM1), which is realistically modelled by genetically engineered CD40L-deficient mice. Neither CD40L-deficient patients nor mice make effective antibodies or mount cellular immune responses that would defend them against intracellular pathogens such as parasites. Consequently, the only potentially curative therapy is allogeneic stem cell transplantation or CD40L gene replacement. Here, we used a retroviral vector, which constitutively expressed CD40L, to genetically modify CD40L-deficient bone marrow cells, which were used to reconstitute partially the immunity of CD40L-deficient mice. The crucial importance of tight regulation of CD40L expression was revealed when these mice later developed lethal thymic T cell malignancy. Growing tumours escape immune vigilance by genetic alterations that reduce their sensitivity to IFNγ. Using murine tumour models, we incorporated transgenic CD40L expression in therapeutic tumour vaccines to show that CD40L gene transfer augmented the immunogenicity of the host’s tumour thus reducing its tumorigenicity. We translated this finding clinically to safety and immunogenicity testing of a transgenic CD40L- and IL-2- expressing leukaemia vaccine.
Finally, the common viral respiratory pathogen, respiratory syncytial virus (RSV) mainly infects young infants and the elderly to cause potentially lethal pneumonia. Both groups have reduced cellular and humoral immunity, which predisposes them to re-infection with RSV. Using a murine model, we showed first that simultaneous adenoviral expression of CD40L augmented primary RSV-specific Th1 responses that were associated with accelerated pulmonary viral clearance. Second, we showed that expression of CD40L in RSV-F and RSV-G subunit DNA vaccines elevated antibody and cellular immune responses to RSV challenge four and eight months after the initial immunisation.
These results demonstrate the potent ability of CD40L gene transfer to solve the absolute immune deficiency caused by genetic lesions of CD40L. However, physiological regulation of the transgene is required to prevent serious adverse consequences. In contrast, no adverse effects were observed after transgenic CD40L expression was used to overcome relative immune deficiencies imposed by malignancy and RSV infection.Thesis (Ph.D.) - University of Adelaide, School of Medicine, 2007
Books on the topic "Immunogenetics (incl. Genetic Immunology)"
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1951-, Barnett A. H., ed. Immunogenetics of insulin-dependent diabetes. Lancaster: MTP Press, 1987.
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J, Goodacre, and Dick W. Carson, eds. Immunopathogenetic mechanisms of arthritis. Lancaster: MTP Press, 1988.
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A, Jaworski Martine, ed. The immunology of diabetes mellitus: Proceedings of the International Symposium on the Immunology of Diabetes, Edmonton, 26-28 June 1986. Amsterdam: Excerpta Medica, 1986.
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Wayne, Streilein J., ed. Advances in gene technology: Molecular biology of the immune system : proceedings of the Seventeenth Miami Winter Symposium, Miami, Florida, U.S.A., February 11-15, 1985. Cambridge: Cambridge University Press, 1985.
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Bone marrow transplantation across major genetic barriers. Hackensack, New Jersey [u.a.]: World Scientific, 2010.
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Derek, Wakelin, and Blackwell J. M, eds. Genetics of resistance to bacterial and parasitic infection. London: Taylor & Francis, 1988.
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Mak, Tak W. Handbook of immune response genes. New York: Plenum Press, 1998.
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Michael, Browning, and McMichael Andrew J, eds. HLA and MHC: Genes, molecules and function. Oxford: BIOS Scientific, 1996.
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Oksenberg, Jorge R., and David Brassat. Immunogenetics of Autoimmune Disease. Springer, 2014.
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(Editor), Jorge R. Oksenberg, and David Brassat (Editor), eds. Immunogenetics of Autoimmune Disease (Medical Intelligence Unit). Springer, 2006.
Find full textBook chapters on the topic "Immunogenetics (incl. Genetic Immunology)"
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Nepom, G. T. "Reverse Immunogenetics: Investigations of HLA-Associated Disease Based on the Structural and Genetic Identification of Candidate Susceptibility Genes." In Progress in Immunology, 805–12. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-83755-5_109.
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