Letteratura scientifica selezionata sul tema "Immune response Molecular aspects"
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Articoli di riviste sul tema "Immune response Molecular aspects"
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AS, Dr Maniyammai, Dr Amudha M, Dr Renuka Devi R, Dr Esther Nalini H e Dr Arun Kumar Prasad. "Adaptive immune response: Molecular aspects of periodontal disease". International Journal of Applied Dental Sciences 7, n. 4 (1 ottobre 2021): 89–92. http://dx.doi.org/10.22271/oral.2021.v7.i4b.1356.
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Goodman, Jesse L. "Molecular Aspects of Immune Response in Infectious Diseases". Clinical Infectious Diseases 13, n. 3 (1 maggio 1991): 530. http://dx.doi.org/10.1093/clinids/13.3.530-a.
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Inman, R. D. "Immunogenetic aspects of host immune response". Canadian Journal of Microbiology 34, n. 3 (1 marzo 1988): 319–22. http://dx.doi.org/10.1139/m88-058.
Testo completoAbstract (sommario):
The central role of histocompatibility leukocyte antigens (HLA) class II molecules in antigen presentation has received great attention in recent years, yet class I molecules have been defined as primarily functioning as a restriction element for cytotoxic T cell killing of virus-infected cells. Extensive clinical evidence, however, indicates that the HLA class I genes are strongly associated with nonseptic complications of enteric and genitourinary bacterial infections. Ninety percent of patients with Reiter's syndrome and reactive arthritis are positive for HLA-B27, yet the mechanism of disease susceptibility conferred by this gene remains obscure. Hypotheses concerning this interaction include (i) class I antigens functioning as receptors for microbial antigens; (ii) class I antigens expressing determinants that cross-react with microbial antigens; and (iii) class I genes controlling immunoregulatory functions that dictate qualitative differences in immune response to pathogenic organisms. These hypotheses await formal testing and hold great promise for understanding immunogenetic control of immune responses in general.
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Jeffries, Donald. "Book Review: Molecular Aspects of Immune Response and Infectious Diseases". International Journal of STD & AIDS 2, n. 3 (maggio 1991): 218. http://dx.doi.org/10.1177/095646249100200322.
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Stetson, C. A., e E. Jensen. "HUMORAL ASPECTS OF THE IMMUNE RESPONSE TO HOMOGRAFTS *". Annals of the New York Academy of Sciences 87, n. 1 (15 dicembre 2006): 249–57. http://dx.doi.org/10.1111/j.1749-6632.1960.tb23198.x.
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INNES, ELISABETH A., DAVID BUXTON, STEPHEN MALEY, STEPHEN WRIGHT, JOANNE MARKS, IRMA ESTEBAN, ALISTAIR RAE, ALEX SCHOCK e JONATHAN WASTLING. "Neosporosis: Aspects of Epidemiology and Host Immune Response". Annals of the New York Academy of Sciences 916, n. 1 (25 gennaio 2006): 93–101. http://dx.doi.org/10.1111/j.1749-6632.2000.tb05278.x.
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Sonenshine, Daniel, E. "Molecular characterization and related aspects of the innate immune response in ticks". Frontiers in Bioscience Volume, n. 13 (2008): 7046. http://dx.doi.org/10.2741/3209.
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Nikolic, Dejan, Milena Jankovic, Bojana Petrovic e Ivana Novakovic. "Genetic Aspects of Inflammation and Immune Response in Stroke". International Journal of Molecular Sciences 21, n. 19 (8 ottobre 2020): 7409. http://dx.doi.org/10.3390/ijms21197409.
Testo completoAbstract (sommario):
Genetic determinants play important role in the complex processes of inflammation and immune response in stroke and could be studied in different ways. Inflammation and immunomodulation are associated with repair processes in ischemic stroke, and together with the concept of preconditioning are promising modes of stroke treatment. One of the important aspects to be considered in the recovery of patients after the stroke is a genetic predisposition, which has been studied extensively. Polymorphisms in a number of candidate genes, such as IL-6, BDNF, COX2, CYPC19, and GPIIIa could be associated with stroke outcome and recovery. Recent GWAS studies pointed to the variant in genesPATJ and LOC as new genetic markers of long term outcome. Epigenetic regulation of immune response in stroke is also important, with mechanisms of histone modifications, DNA methylation, and activity of non-coding RNAs. These complex processes are changing from acute phase over the repair to establishing homeostasis or to provoke exaggerated reaction and death. Pharmacogenetics and pharmacogenomics of stroke cures might also be evaluated in the context of immuno-inflammation and brain plasticity. Potential novel genetic treatment modalities are challenged but still in the early phase of the investigation.
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Petean, Igor Bassi Ferreira, Alice Corrêa Silva-Sousa, Tamara Justiniano Cronenbold, Jardel Francisco Mazzi-Chaves, Lea Assed Bezerra da Silva, Raquel Assed Bezerra Segato, Guilherme Assed Piedade de Castro, Erika Calvano Kuchler, Francisco Wanderley Garcia Paula-Silva e Manoel Damião Sousa-Neto. "Genetic, Cellular and Molecular Aspects involved in Apical Periodontitis". Brazilian Dental Journal 33, n. 4 (agosto 2022): 1–11. http://dx.doi.org/10.1590/0103-6440202205113.
Testo completoAbstract (sommario):
Abstract The development, establishment and repair of apical periodontitis (AP) is dependent of several factors, which include host susceptibility, microbial infection, immune response, quality of root canal treatment and organism's ability to repair. The understanding of genetic contributions to the risk of developing AP and presenting persistent AP has been extensively explored in modern Endodontics. Thus, this article aims to provide a review of the literature regarding the biochemical mediators involved in immune response signaling, osteoclastogenesis and bone neoformation, as the genetic components involved in the development and repair of AP. A narrative review of the literature was performed through a PUBMED/MEDLINE search and a hand search of the major AP textbooks. The knowledge regarding the cells, receptors and molecules involved in the host's immune-inflammatory response during the progression of AP added to the knowledge of bone biology allows the identification of factors inherent to the host that can interfere both in the progression and in the repair of these lesions. The main outcomes of studies evaluated in the review that investigated the correlation between genetic polymorphisms and AP in the last five years, demonstrate that genetic factors of the individual are involved in the success of root canal treatment. The discussion of this review gives subsides that may help to glimpse the development of new therapies based on the identification of therapeutic targets and the development of materials and techniques aimed at acting at the molecular level for clinical, radiographic and histological success of root canal treatment.
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McNamara, Mairéad G., Jean-Yves Scoazec e Thomas Walter. "Extrapulmonary poorly differentiated NECs, including molecular and immune aspects". Endocrine-Related Cancer 27, n. 7 (luglio 2020): R219—R238. http://dx.doi.org/10.1530/erc-19-0483.
Testo completoAbstract (sommario):
Patients with extrapulmonary poorly differentiated neuroendocrine carcinomas (EP-PD-NECs) have a poor prognosis. Surgery is offered for those with localised disease, but the majority of patients present with advanced disease. Treatment strategies adopted are analogous to that of high grade NECs of the lung, with platinum/etoposide-based regimens advocated in the first-line setting for advanced disease. There is no standard second-line therapy. Research into their molecular and immune pathways may pave the way for novel drug discovery. The molecular drivers of NEC are best identified in small cell lung carcinoma, which present with near universal genomic alterations in TP53 and RB1. The genetics of EP-PD-NEC remain poorly understood; TP53, KRAS, PIK3CA/PTEN and BRAF mutations have been identified, with alterations in the BRCA pathway reported additionally in small cell NEC of the cervix and absence of argininosuccinate synthetase 1 expression in NEC of the urinary bladder. The use of cell lines and patient-derived xenografts (PDX) to predict response to treatment in NEC and the emergence of alternative biomarkers, such as circulating tumour cells and cell-free DNA, will also be explored. Despite limited published data on the immune microenvironment of EP-NEC, there are a number of clinical trials investigating the use of immune-targeted agents in this disease category, with conflicting emerging data from studies thus far. This review will summarise the treatment and available molecular and immune data in this under researched diagnosis and may stimulate the direction of future exploratory studies.
Tesi sul tema "Immune response Molecular aspects"
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Morley, Sarah Louise. "Molecular aspects of the humoral immune response against Neisseria meningitidis". Thesis, Imperial College London, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.424765.
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Wong, Lik-wai Benny, e 黃力偉. "Immune response and signaling mechanisms of Helicobacter pylori induced gastritis". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B43224313.
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Prabhala, Rao H. "Two different molecular pathways of immunomodulation by retinoids and carotenoids". Diss., The University of Arizona, 1989. http://hdl.handle.net/10150/184676.
Testo completoAbstract (sommario):
Epidemiological studies suggest that both retinoid and carotenoid intakes are inversely correlated with the incidence of human cancers. Animal studies show that both retinoids and carotenoids inhibit tumor cell growth. Both retinoids and carotenoids activate the cytotoxicity function of macrophages in animal experiments. The purpose of this study is to evaluate the molecular mechanism for 13-cis retinoic acid (13-cRA) and beta-carotene (BC) induced immunomodulation which could explain their anti-cancer affects. The effects of 13-cRA and BC were studied on various subpopulations of T-lymphocytes both in vitro and in vivo. For in vitro studies, peripheral blood mononuclear cells (PBMC) were incubated with test compounds at clinically achievable concentrations (10⁻⁸M) for three days. Then the cells were stained with monoclonal antibodies followed by the analysis of flow cytometer. For in vivo studies, PBMC were collected from Barrett's esophagus or oral leukoplakia patients during treatment with 13-cRA (1mg/kg/day) or BC (30 mg/day), respectively. Then the cells were analyzed with monoclonal antibodies and flow cytometry. Both compounds showed the capability of stimulating different subpopulations of T-lymphocytes. 13-cRA predominantly increased the number of T-helper cells, their interleukin 2 (IL-2) receptors and their response to mitogens. Whereas, BC elevated the number of Natural Kill (NK) cells, their IL-2 receptors and their cytotoxicity against K562 target cells. Though these immunomodulatory effects appeared to be unaffected by the presence and cytotoxic functions of macrophages, cytokines seemed to have an important role in the retinoid- and carotenoid-induced immunomodulation. Plasma levels of IL-2 and tumor necrosis factor (TNF) measured by ELISA procedures were increased in patients treated for two months with 13-cRA and BC respectively. Anti-IL-2 and anti-TNF antibodies blocked the retinoic- and carotenoid-induced immunomodulation in in vitro studies. These results indicate that 13-cRA, activating T-helper cells with IL-2 production, and BC, activating NK cells with TNF release, induced immunostimulation which might be able to provide the anti-cancer affects in part seen in epidemiological studies.
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Swanson, Kara M., e n/a. "The bovine mammary gland immune response to Streptococcus uberis and its bacteriocins". University of Otago. Department of Microbiology & Immunology, 2008. http://adt.otago.ac.nz./public/adt-NZDU20080407.112302.
Testo completoAbstract (sommario):
Bovine mastitis is one of the most costly dairy-based diseases worldwide. Streptococcus uberis is a prevalent causative organism of mastitis and resides naturally in the environment of the dairy cow making prevention of the disease difficult. New strategies need to be developed to control this pathogen. However, a fundamental understanding of the complex relationships that exist between the cow, the pathogen and the environment are required in order to advance the development of prevention strategies. Microarray technology was used to evaluate the complex transcriptional changes which occur in the bovine mammary gland following the onset of clinical S. uberis mastitis. A 22,000 bovine cDNA microarray indicated that S. uberis mastitis led to the up-regulation of 1,283 genes and the down-regulation of 1,237 genes by greater than 1.5 fold. Gene ontology analysis demonstrated that S. uberis mastitis was typically associated with the up-regulation of genes that are involved in the immune response and homeostasis and a down-regulation of genes involved in lipid metabolism. Quantitative real-time analyses for a selection of genes associated with the immune response validated the microarray data. Mammary epithelial cell cultures did not show an increase in the expression of any of these immune factors in response to the same S. uberis strain used to induce clinical mastitis. This indicates that the expression of immune-related genes by mammary epithelial cells may be initiated by host factors and not S. uberis.
The application of bacteriocins, proteinaceous antimicrobials produced by bacteria which typically inhibit the same or closely-related species to that of the producer organism, has been suggested as one possible approach in the control of mastitis. S. uberis have been previously found to commonly produce bacteriocin-like inhibitory substances (BLIS). The BLIS activities of a set of fifteen S. uberis and S. bovis strains were assessed. The results confirmed the prolific and varied nature of BLIS production by S. uberis and S. bovis and also indicated that these strains may commonly produce more than one inhibitory agent. This survey of BLIS production led to the detection and characterisation of a novel circular bacteriocin, uberolysin, produced by S. uberis strains 233 and 42. The structural gene of uberolysin was subsequently identified in nine (64%) of the fifteen test strains.
Multiplex PCR analysis showed that 93% of 158 New Zealand S. uberis isolates contained the structural genes of at least one of the four known S. uberis bacteriocins (uberolysin, nisin U, ubericin A and ubericin 63). However, no apparent direct association was identified between any one of these bacteriocin-related loci and apparent ability to cause mastitis on New Zealand dairy farms. The uberolysin structural gene was detected in 91% of the isolates and this widespread distribution prompted the advancement and evaluation of a potential role for uberolysin in immunomodulation within the bovine mammary gland. Two different preparations of uberolysin were found to have different stimulatory effects on monocytes, neutrophils and epithelial cells. The less highly purified preparation appeared to diminish the production of TNF-α by monocytes in the presence of a bacterial stimulus and to decrease neutrophil phagocytosis. By contrast, the relatively more highly purified preparation of uberolysin itself induced a significant immune response by monocytes. Consistent with this, the purer preparation of uberolysin induced an increase in C3, IL-1β, IL-6, IL-8, the β-defensin LAP, the acute-phase protein MSAA, the calcium-binding protein S100A12 and TLR2 by quantitative real-time analysis.
Although currently only two S. uberis bacteriocins (uberolysin and nisin U) have been fully characterised, the present study has shown that this species may be an important source of novel antimicrobials. Furthermore, bacteriocin production by S. uberis may have an immunomodulation role within the mammary gland. A better understanding of the complex immune response initiated at the onset of clinical S. uberis mastitis and of the role that bacteriocins have in S. uberis pathogenesis may lead to development of improved strategies to combat this disease.
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Chakravarti, Sumone. "The cloning and functional characterisation of murine phosphatidylinositol 3-kinase gamma". Title page, table of contents and abstract only, 2001. http://web4.library.adelaide.edu.au/theses/09PH/09phc4355.pdf.
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Mooney, John. "Molecular and cellular aspects of the humoral immune response in periodontal disease and other related conditions". Thesis, University of Glasgow, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.321510.
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Sumaria, Nital. "The relevance of specific molecular and cellular effectors during murine cytomegalovirus infection". University of Western Australia. School of Biomedical, Biomolecular and Chemical Sciences, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0116.
Testo completoAbstract (sommario):
[Truncated abstract] The design and development of effective anti-viral immunotherapies requires a comprehensive understanding of the cellular and molecular processes that are involved in the generation and regulation of immune responses. The fundamental objective of the immune system is to successfully complete the task of eliminating/controlling the invading pathogen without causing overt pathology. Cytomegaloviruses (CMVs) are large DNA viruses that are able to evade immune attack and persist lifelong within the host. In a healthy host, CMV causes an asymptomatic infection, but in instances of decreased immune functions, such as in newborns, acquired immunodeficiency syndrome (AIDS) patients and transplant recipients, the infection can result in serious morbidity and mortality. Thus, human CMV (HCMV) is a clinically important pathogen and an understanding of the pathogenesis, mechanisms of immune subversion and, importantly the cascade of immune events that ensue following infection is highly relevant. The studies presented in this thesis have provided useful insight into various aspects of viral immunity and it is hoped that they will assist in the design of more effective therapies against viruses of clinical importance. Genetic variability in humans can greatly influence anti-viral immune responses and the outcome of viral infection. ... Furthermore, these studies provide novel evidence that NK cells are also crucial for the control of virus in some organs of susceptible mice during early acute infection. The data reveals that both NK cells and CD8+ T cells utilise perforin- and IFN-? dependent control of MCMV. Furthermore, these studies provide novel evidence that protection mediated by Ly49H+ NK cells in resistant mice is dependent on perforin. Chapter 3 focuses on the biological relevance of Grz during MCMV infection. These studies found that GrzA and GrzB are essential components of the machinery involved in limiting MCMV during acute infection. These analyses also provide the first evidence suggesting that GrzM plays a role, albeit minor, in controlling MCMV replication. Furthermore, the current studies suggest that Grz can mediate direct antiviral activities independent of the induction of cell death in conjunction with perforin. Interestingly, in the absence of both GrzA and GrzB (GrzAB), mice were as susceptible to MCMV infection as perforin-deficient mice. However, unlike perforin-deficient mice, GrzAB-deficient mice controlled and survived the infection. In Chapter 4 the roles of perforin, GrzA and GrzB in anti-viral immunity and immunopathology during MCMV infection were examined. These studies show that NK cell-derived perforin is required to eliminate infected targets as well as activated effector cells, suggesting that NK cells are crucial not only in defensive immunity but also in limiting the immune activation that follows MCMV infection. In summary, the studies presented in this thesis define the significant role played by specific effector molecules in limiting MCMV replication during different stages of this viral infection. Furthermore, these studies provide novel evidence that perforin, GrzA and GrzB play distinct roles in defensive immunity and limiting immunopathology during MCMV infection.
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Andrews, Daniel Mark. "Effects of murine cytomegalovirus infection on dendritic cell functionality and natural killer cell responses". University of Western Australia. Centre for Ophthalmology and Visual Science, 2004. http://theses.library.uwa.edu.au/adt-WU2005.0003.
Testo completoAbstract (sommario):
Cytomegaloviruses (CMVs) are ubiquitous in nature, having evolved over many millenia with their hosts. While in healthy hosts most infections with CMV are asymptomatic, the virus can cause severe disease in immunocompromised hosts. Thus, the increase in organ transplantation and the HIV/AIDS pandemic have established human CMV (HCMV) as a clinically important pathogen. Indeed, HCMV infections are now the major cause of morbidity and mortality among immunocompromised patients, which has led to more research targeting CMV for effective anti-viral treatment. The discovery that cytomegaloviruses encode several genes which are involved in immune escape has prompted a new area of research, aimed at understanding immune escape mechanisms for exploitation as potential anti-viral therapeutics. By targeting the viral proteins directly, or their receptors in the host, it may be possible to treat CMV disease by agonistic/antagonistic therapy. The first part of this thesis describes the first demonstration of anti-NK1.1 staining in situ to identify NK cells using a modified in vivo perfusion/fixation method. Using this method, we have compared the acute NK1.1+ cellular response to wild-type MCMV infection in the visceral organs of genetically susceptible intra-NK complex recombinant BALB.B6-CT6 (Cmv1s, NK1.1+) mice with resistant C57B⁄J (Cmv1r, NK1.1+) and BALB.B6-Cmv1r mice (Cmv1r, NK1.1+). Expression of viral antigens and the consequences of infection on other cellular subsets, were also analyzed in this study. The data show that in susceptible mice (Cmv1s) MCMV infection is predominent in the marginal zone of splenic white pulp, resulting in local changes in various cellular constituents, including macrophages, NK cells and DC. In the liver, distinct foci of infection were comprised of large numbers of macrophages and NK1.1+ cells surrounding infected cytomegalic cells. In resistant mice (Cmv1r), 6 MCMV infection predominantly affected the red-pulp of the spleen and was associated with increased accumulation of NK1.1+ cells and macrophages at sites of viral infection
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Kodituwakku, Aruna Poojitha. "Antigen specific B cells in the immune response to Haemophilus influenzae type b PRP conjugate vaccine /". Title page, table of contents and summary only, 2004. http://web4.library.adelaide.edu.au/theses/09PH/09phk769.pdf.
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Khong, Andrea. "Effect of murine cytomegalovirus infection on haematopoiesis and myeloid cell differentiation and function". University of Western Australia. School of Biomedical, Biomolecular and Chemical Sciences, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0260.
Testo completoAbstract (sommario):
Cytomegalovirus (CMV) is a ubiquitous pathogen affecting over 95% of the worlds population. While infection is typically asymptomatic in healthy individuals, the virus persists life-long in its host and can be reactivated following withdrawal of immune control. As such, it remains a serious clinical concern in individuals who are immunocompromised, such as newborns and neonates, transplant and/or chemotherapy recipients, and HIV/AIDS patients. CMV also has the ability to cause immunosuppression, the mechanisms of which include defective antigen presentation to T cells and interference with haematopoiesis in the bone marrow (BM). Due to strict species specificity, murine CMV (MCMV) provides a relevant model for the study of CMV modulation of the immune system in vivo in its natural host. The type I interferons (IFNs) represent a major family of cytokines involved in the early response to MCMV infection. Their anti-viral activity and regulation of NK cell activation and cytotoxicity are of significant interest in the context of MCMV infection, as genetic resistance to MCMV is mediated by the ability of Ly49H+ NK cells to directly recognise and lyse infected cells. Chapter 2 comprises an analysis of acute MCMV infection in the absence of type I IFN activity. These studies were conducted in IFNAR1 and IFNAR2 deficient mice, which lack components of the type I IFN receptor. Data obtained from these studies confirmed the essential requirement for type I IFN in controlling viral titres, promoting expansion of splenic Ly49H+ NK cells, and inducing early activation of NK cell cytotoxicity. In addition, our data depicted an accumulation of infected myeloid cells in the absence of effective NK cell-mediated control. This was paralleled by a significant increase in the level of serum TNF-a and IFN-¿, an effect which in some cases has been linked to serious pathological disease. Thus, the data described in this chapter provide an insight into the consequences arising from delayed NK cell responses to MCMV infection in the absence of type I IFN. vii Type I IFN can also potentially affect BM haematopoiesis. BM atrophy and impairment of myelopoiesis are serious consequences of CMV infection. During acute MCMV infection we consistently observed a profound loss of splenic dendritic cells (DCs) in BALB/c mice. Since all DC subsets are derived from BM haematopoietic progenitor cells, the possibility that MCMV might interfere with BM haematopoiesis and DC differentiation was explored. Chapters 3 and 4 describe the impact of acute MCMV infection on BM progenitors, with particular emphasis on the differentiation capabilities of these cells in ex vivo culture systems. Chapter 3 focuses on the effect of MCMV infection on BM cellularity and frequency of specific BM progenitor populations. A thorough analysis of contributing factors, such as viral infection of BM cells, involvement of type I and II IFNs, progenitor cell trafficking and NK cell activity in the BM compartment, was conducted. Our results showed that a severe loss of BM cellularity occurs in MCMV-infected mice. Furthermore, when BM cells from MCMV-infected mice were cultured ex vivo in granulocyte macrophage-colony stimulating factor (GM-CSF), there was an impairment in their ability to differentiate into DCs.
Libri sul tema "Immune response Molecular aspects"
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1956-, Srivastava Rakesh, Ram Bhanu P. 1951- e Tyle Praveen 1960-, a cura di. Molecular mechanisms of immune regulation. New York, N.Y: VCH Publishers, 1991.
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Delʹvig, A. A. Kletochnye i molekuli︠a︡rnye osnovy prezentat︠s︡ii antigenov. Moskva: Medit︠s︡ina, 2004.
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Wayne, Streilein J., a cura di. Advances in gene technology: The molecular biology of immune diseases and the immune response : proceedings of the 1990 Miami Bio/Technology Winter Symposia. Oxford: IRL Press at Oxford University Press, 1990.
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Mak, Tak W. Handbook of immune response genes. New York: Plenum Press, 1998.
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Miami Bio/Technology Winter Symposia (1990). Advances in gene technology: The molecular biology of immune diseases and the immune response : proceedings of the 1990 Miami Bio/Technology Winter Symposia. Oxford ; New York: IRL Press at Oxford University Press, 1990.
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Green Cross International Symposium (1st 1992 Kyoto). Molecular basis of immune responses: [proceedings of the First Green Cross International Symposium "immunology for tomorrow" 1992]. Tokyo: Academic Press, 1993.
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Miami Bio/Technology Winter Symposium (1990 Miami, Fla.). Advances in gene technology: The molecular biology of immune diseases and the immune reponse : proceedings of the 1990 Miami Bio/Technology Winter Symposia. Oxford: IRL Press, 1990.
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Donata, Vercelli, a cura di. IgE regulation: Molecular mechanisms. Chichester: J. Wiley, 1997.
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Akira, Wake. Host-parasite relationships and the Yersinia model. New York: Springer-Verlag, 1986.
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D, Batista Facundo, e SpringerLink (Online service), a cura di. Immunological Synapse. Berlin, Heidelberg: Springer-Verlag Berlin Heidelberg, 2010.
Cerca il testo completoCapitoli di libri sul tema "Immune response Molecular aspects"
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Liu, G., A. Keane-Myers, D. Miyazaki, A. Tai e S. J. Ono. "Molecular and Cellular Aspects of Allergic Conjunctivitis". In Immune Response and the Eye, 39–58. Basel: KARGER, 1999. http://dx.doi.org/10.1159/000058748.
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McFarland, Henry F., e Steven Jacobson. "The Immune Response to Viruses". In Clinical and Molecular Aspects of Neurotropic Virus Infection, 469–99. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-1675-6_17.
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Milich, David R. "Molecular and Genetic Aspects of the Immune Responses to Hepatitis B Viral Antigens". In The Immune Response to Viral Infections, 115–33. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-5712-4_12.
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Tavasolian, Fataneh, Gholam Reza Hatam, Sayed Hussain Mosawi, Mahdiyar Iravani Saadi, Elham Abdollahi, Tannaz Jamialahmadi, Thozhukat Sathyapalan e Amirhossein Sahebkar. "The Immune Response and Effectiveness of COVID-19 Therapies". In Clinical, Biological and Molecular Aspects of COVID-19, 115–26. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-59261-5_10.
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Spiegel, Allen M. "Guanine Nucleotide Regulatory Proteins in Inflammatory and Immune Responses". In Cellular and Molecular Aspects of Inflammation, 209–27. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4684-5487-1_11.
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Siliciano, R. F. "Molecular Aspects of Human B and T Lymphocyte Responses to HIV". In Herpesviruses, the Immune System, and AIDS, 45–71. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4613-1507-0_3.
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Neagu, Monica, e Carolina Constantin. "Signal Transduction in Immune Cells and Protein Kinases". In Advances in Experimental Medicine and Biology, 133–49. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-49844-3_5.
Testo completoAbstract (sommario):
AbstractImmune response relies upon several intracellular signaling events. Among the protein kinases involved in these pathways, members of the protein kinase C (PKC) family are prominent molecules because they have the capacity to acutely and reversibly modulate effector protein functions, controlling both spatial distribution and dynamic properties of the signals. Different PKC isoforms are involved in distinct signaling pathways, with selective functions in a cell-specific manner.In innate system, Toll-like receptor signaling is the main molecular event triggering effector functions. Various isoforms of PKC can be common to different TLRs, while some of them are specific for a certain type of TLR. Protein kinases involvement in innate immune cells are presented within the chapter emphasizing their coordination in many aspects of immune cell function and, as important players in immune regulation.In adaptive immunity T-cell receptor and B-cell receptor signaling are the main intracellular pathways involved in seminal immune specific cellular events. Activation through TCR and BCR can have common intracellular pathways while others can be specific for the type of receptor involved or for the specific function triggered. Various PKC isoforms involvement in TCR and BCR Intracellular signaling will be presented as positive and negative regulators of the immune response events triggered in adaptive immunity.
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High, Kevin P. "Immune Senescence". In Molecular Aspects of Aging, 85–97. Hoboken, NJ: John Wiley & Sons, Inc, 2014. http://dx.doi.org/10.1002/9781118396292.ch7.
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Marion, James. "Immunology and the Immune Response". In Molecular Life Sciences, 1–5. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-6436-5_648-1.
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Marion, James. "Immunology and the Immune Response". In Molecular Life Sciences, 539–43. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4614-1531-2_648.
Testo completoAtti di convegni sul tema "Immune response Molecular aspects"
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Kolubako, A. V., e Y. A. Nikolaichik. "Molecular aspects of Pectobacterium carotovorum – Solanum tuberosum interaction". In 2nd International Scientific Conference "Plants and Microbes: the Future of Biotechnology". PLAMIC2020 Organizing committee, 2020. http://dx.doi.org/10.28983/plamic2020.124.
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Silva, Tarcisio Rubens da, Marina Monteiro Navarro, Mylena Mendes Hóstio e Catherine Sonaly Ferreira Martins. "Case report - Ataxia-telangiectasia: innate error of immunity and neurological aspects". In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.233.
Testo completoAbstract (sommario):
Introduction: Among more than 350 immunological deficiencies, 25% have neurological manifestations. Thus, Ataxia-telangiectasia stands out, being considered a combined immunodeficiency. In childhood, cerebellar motor findings and recurrent sinopulmonary infections, signaling early cerebellar degeneration and deficit in the combined immune response. It has an autosomal recessive inheritance pattern. Case report: She describes herself as a female patient, 9 years old, daughter of consanguineous parents and born in Sousa, Paraíba. In the child’s neuropsychomotor development, she sat down at 5 months, verbalized loose words at 12 months and started the process of ambulation at 13 months of life. While walking, the mother noticed strange walking and frequent hospitalizations due to recurrent pneumonia. From 7 years of age, there is worsening of gait and telangiectasias in the conjunctiva are evident. Subsequently, the molecular examination in order to demonstrate the possible mutation. Therefore, a mutation described as c.7913G> A (p.Trp2638 *) was found in homozygosity in exon 53 of the ATM gene. Findings: typical onset of early childhood when walking, swallowing problems with solid and liquid foods and the growth disorder. Regarding the immune system: low levels of immunoglobulins, but without lymphopenia and the worrying presence of adenomegaly, making it necessary to always pay attention to neoplasms such as leukemias and lymphomas. In disagreement, there are no: myoclonus, the highest IgM levels, cutaneous granulomas and bone deformities. Conclusions: The case presents aspects that are very consistent with the scientific findings consolidated in Ataxia-telangiectasia, but the late molecular diagnosis.
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Silva, Gustavo Figueiredo da, Caroline Figueiredo da Silva, Washigton Luiz Gomes de Medeiros Junior e Marcus Vinícius Magno Gonçalves. "Anti -Iglon5 Syndrome: What we know so far? A non-systematic review". In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.237.
Testo completoAbstract (sommario):
Background: The first report of Anti-IgLON5 syndrome was in 2014. AntiIgLON5 antibodies have a prevalence of 12 in 150,000 patients per year. However, considering the unreported patients, the prevalence can be much higher. Objectives: Provide an overview of the current knowledge of Anti- IgLON5 syndrome. Design and setting: Narrative review. Methods: Non- systematic review on Pubmed database. Results: The IgLON proteins are a family of cell adhesion molecules and the presence of antibodies against IgLON5 is crucial for the AntiIgLON5 Syndrome diagnosis. This syndrome has an expanded clinical spectrum that involves prominent sleep disorder, progressive bulbar dysfunction, gait instability with abnormal eye movements reminiscent, and cognitive deterioration sometimes associated with chorea. The main neuropathological finding is the neuronal loss with hyperphosphorylated tau protein accumulation at the hypothalamus, brainstem tegmentum, hippocampus, periaqueductal gray matter, medulla oblongata, and upper cervical cord. The exact pathogenesis is still unclear and involves a neurodegenerative process and autoimmune response. Early diagnosis is important to avoid unnecessary tests and prevent complications. Important resources for diagnosis are the antibody testing of serum and cerebrospinal fluid for IgLON5-IgG. The Anti-IgLON5 syndrome mortality is high and new studies published described a good response to immune therapy, however, depends on some clinical and analytical characteristics. Conclusions: The Anti-Iglon5 syndrome is a pathology still poorly studied and described in the medical literature (only in case series, for example), being a syndrome probably underdiagnosed. Future studies are needed to thoroughly analyze the aspects of pathogenesis and treatment of this important pathological syndrome.
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Krasnoshtanova, Alla, e Alesya Yudina. "PRODUCTION OF ANTIBODIES FROM POULTRY YOLK (IgY) AND INVESTIGATION OF THEIR IMMUNOCHEMICAL PROPERTIES". In GEOLINKS Conference Proceedings. Saima Consult Ltd, 2021. http://dx.doi.org/10.32008/geolinks2021/b1/v3/17.
Testo completoAbstract (sommario):
"A particularly important aspect of immunology is to develop non-invasive methods of obtaining antibodies which could be a great alternative to traditional ones that based on the harmful procedure of isolation of immunoglobulins from animal blood sera. That’s why the extraction of antibodies from poultry egg yolks (IgY) is the most promising. Due to the fact of variation of IgY structural features that determine the definite immunochemical properties, yolk antibodies in comparison with mammalian immunoglobulins (IgG) does not interact with rheumatoid factor (Rf), contribute to the activation of the complement system, bind to the Fc-receptor (FcR), and also has weak cross-reactivity, which confirms the possibility of their widespread use in medicine and food. Also the presence of phylogenetic distance between chickens and mammalians guarantees immune response against conservative mammalian protein molecules which is highly important for the creation of new generation test systems. The aim of this work is to develop a selective method of producing high-purity immunoglobulin Y preparations from the yolk of chicken eggs. There were adopted selective conditions of isolation of IgY under spontaneous thawing procedure at the room temperature of firstly frozen yolk solution in a sodium-phosphate buffer mixed with water (pH 5.0) in a ratio of 1:6, which leads to receiving a water-soluble fraction further precipitated with the sodium chloride at a concentration of 10% of the solution mass and subsequently concentrated using ultrafiltration with membrane UAM-10, that allows achieving the content of IgY not less than 95% per dry substance in immunoglobulin fraction. It is possible to produce a protein fraction with a protein content of at least 9 g/l. The purity of the immunoglobulin fraction was verified using polyacrylamide gel electrophoresis. The presence of a light chain in the IgY solution was proved to be a low-molecular compound using the method of gel-filtration-chromatography. The immunological activity of IgY was studied with respect to bovine serum albumin (BSA) as an antigen. The enzymatic resistance of IgY against proteolytic enzymes was tested in area of the gastrointestinal tract."
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Aaron, Jesse S., Bryan D. Carson e Jerilyn Timlin. "Simultaneous, Dual-Color STORM Imaging of Membrane Reorganization during Early Immune Response". In Optical Molecular Probes, Imaging and Drug Delivery. Washington, D.C.: OSA, 2011. http://dx.doi.org/10.1364/omp.2011.oma3.
Testo completo
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Coukos, George. "Abstract KN01: Dissecting antitumor immune response in ovarian cancer". In Abstracts: AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics; October 26-30, 2019; Boston, MA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1535-7163.targ-19-kn01.
Testo completo
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Yang, Ivana V., Laura A. Warg, Elizabeth J. Davidson, Samir N. P. Kelada, Kari Kubalanza, Francis S. Collins, Elissa J. Chesler et al. "INNATE IMMUNE GENE DISCOVERY USING MACROPHAGE RESPONSE TO PATHOGEN-ASSOCIATED MOLECULAR PATTERNS (PAMPS)". In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a1273.
Testo completo
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Shvaratska, Olha, Yuriy Bolbot e Anna Karpenko. "Some aspects of mucosal immune response in children with bacterial upper respiratory tract infections". In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa1000.
Testo completo
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Lenhardt, Maurício Machado, Dauana Schwartz e Bruna K. de F. Silva. "Can depression be associated with the immune response". In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.443.
Testo completoAbstract (sommario):
Introduction: Depression is a disease of uncertain installation and etiology, the imbalance of neurotransmitters is involved in this process, and stress can be an activator of pro-inflammatory cytokines and trigger depressive symptoms. The organism undergoes modulations due to biochemical changes and these are linked to molecular and biochemical components and by the survival instinct, the human body is stimulated to release substances as a form of protection. The objective of this study is to describe the possible association between a loss of homeostasis of the central nervous system (CNS), changes in the modulation of the immune system, and the development of depressive symptoms. Methods: This is an integrative literature review, available in the virtual health databases: PubMed, MEDLINE, SciELO, and Google Scholar published between the years 2010 to 2020. Results: Studies indicate that cytokines can interfere with the homeostasis of the CNS and that the imbalance of catecholamines and indoleamine is involved in the process of depression. In this sense, studies have focused on neuromodulation by blocking neurotransmitters and neuroreceptors to regulate the immune system. Conclusion: It’s already established that the imbalance in the release and reuptake of neurotransmitters is associated with the onset of the depression, however, current studies show that there may also be an association with the homeostasis of the immune system. Therapeutic protocols aren’t based on the correlation between the immune system and the onset of the disease, so further studies are needed to strengthen this relationship.
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Chiaro, Jacopo, Henna Kasanen, Thomas Whalley, Cristian Capasso, Sara Feola, Mikaela Grönholm, Firas Hamdan et al. "Abstract 1488: Viral molecular mimicry influences the antitumor immune response in murine and human melanoma". In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-1488.
Testo completoRapporti di organizzazioni sul tema "Immune response Molecular aspects"
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Eldar, Avigdor, e Donald L. Evans. Streptococcus iniae Infections in Trout and Tilapia: Host-Pathogen Interactions, the Immune Response Toward the Pathogen and Vaccine Formulation. United States Department of Agriculture, dicembre 2000. http://dx.doi.org/10.32747/2000.7575286.bard.
Testo completoAbstract (sommario):
In Israel and in the U.S., Streptococcus iniae is responsible for considerable losses in various fish species. Poor understanding of its virulence factors and limited know-how-to of vaccine formulation and administration are the main reasons for the limited efficacy of vaccines. Our strategy was that in order to Improve control measures, both aspects should be equally addressed. Our proposal included the following objectives: (i) construction of host-pathogen interaction models; (ii) characterization of virulence factors and immunodominant antigens, with assessment of their relative importance in terms of protection and (iii) genetic identification of virulence factors and genes, with evaluation of the protective effect of recombinant proteins. We have shown that two different serotypes are involved. Their capsular polysaccharides (CPS) were characterized, and proved to play an important role in immune evasion and in other consequences of the infection. This is an innovative finding in fish bacteriology and resembles what, in other fields, has become apparent in the recent years: S. iniae alters surface antigens. By so doing, the pathogen escapes immune destruction. Immunological assays (agar-gel immunodiffusion and antibody titers) confirmed that only limited cross recognition between the two types occurs and that capsular polysaccharides are immunodominant. Vaccination with purified CPS (as an acellular vaccine) results in protection. In vitro and ex-vivo models have allowed us to unravel additional insights of the host-pathogen interactions. S. iniae 173 (type II) produced DNA fragmentation of TMB-8 cells characteristic of cellular necrosis; the same isolate also prevented the development of apoptosis in NCC. This was determined by finding reduced expression of phosphotidylserine (PS) on the outer membrane leaflet of NCC. NCC treated with this isolate had very high levels of cellular necrosis compared to all other isolates. This cellular pathology was confirmed by observing reduced DNA laddering in these same treated cells. Transmission EM also showed characteristic necrotic cellular changes in treated cells. To determine if the (in vitro) PCD/apoptosis protective effects of #173 correlated with any in vivo activity, tilapia were injected IV with #173 and #164 (an Israeli type I strain). Following injection, purified NCC were tested (in vitro) for cytotoxicity against HL-60 target cells. Four significant observations were made : (i) fish injected with #173 had 100-400% increased cytotoxicity compared to #164 (ii) in vivo activation occurred within 5 minutes of injection; (iii) activation occurred only within the peripheral blood compartment; and (iv) the isolate that protected NCC from apoptosis in vitro caused in vivo activation of cytotoxicity. The levels of in vivo cytotoxicity responses are associated with certain pathogens (pathogen associated molecular patterns/PAMP) and with the tissue of origin of NCC. NCC from different tissue (i.e. PBL, anterior kidney, spleen) exist in different states of differentiation. Random amplified polymorphic DNA (RAPD) analysis revealed the "adaptation" of the bacterium to the vaccinated environment, suggesting a "Darwinian-like" evolution of any bacterium. Due to the selective pressure which has occurred in the vaccinated environment, type II strains, able to evade the protective response elicited by the vaccine, have evolved from type I strains. The increased virulence through the appropriation of a novel antigenic composition conforms with pathogenic mechanisms described for other streptococci. Vaccine efficacy was improved: water-in-oil formulations were found effective in inducing protection that lasted for a period of (at least) 6 months. Protection was evaluated by functional tests - the protective effect, and immunological parameters - elicitation of T- and B-cells proliferation. Vaccinated fish were found to be resistant to the disease for (at least) six months; protection was accompanied by activation of the cellular and the humoral branches.
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Chejanovsky, Nor, e Bruce A. Webb. Potentiation of pest control by insect immunosuppression. United States Department of Agriculture, luglio 2004. http://dx.doi.org/10.32747/2004.7587236.bard.
Testo completoAbstract (sommario):
Our original aims were to elucidate the mechanisms through which the immunosuppressive insect virus, the Campoletis sonorensis polydnavirus (CsV) promotes replication of a well-characterized pathogenic virus, the Autographa californica multiple nucleopolyhedrovirus (AcMNPV) in hosts that are mildly or non-permissive to virus replication. According to the BARD panels criticism we modified our short-term goals (see below). Thus, in this feasibility study (one-year funding) we aimed to show that: 1. S. littoralis larvae mount an immune response against a baculovirus infection. 2. Immunosuppression of an insect pest improves the ability of a viral pathogen (a baculovirus) to infect the pest. 3. S. littoralis cells constitute an efficient tool to study some aspects of the anti- viral immune response. We achieved the above objectives by: 1. Finding melanized viral foci upon following the baculoviral infection in S . littoralis larvae infected with a polyhedra - positive AcMNPV recombinant that expressed the GFP gene under the control of the Drosophila heat shock promoter. 2. Studying the effect of AcMNPV-infection in S . littoralis immunosuppressed by parasitation with the Braconidae wasp Chelonus inanitus that bears the CiV polydna virus, that resulted in higher susceptibility of S. littoralis to AcMNPV- infection. 3. Proving that S. littoralis hemocytes resist AcMNPV -infection. 4. Defining SL2 as a granulocyte-like cell line and demonstrating that as littoralis hemocytic cell line undergoes apoptosis upon AcMNPV -infection. 5. Showing that some of the recombinant AcMNPV expressing the immuno-suppressive polydna virus CsV- vankyrin genes inhibit baculoviral-induced lysis of SL2 cells. This information paves the way to elucidate the mechanisms through which the immuno- suppressive polydna insect viruses promote replication of pathogenic baculoviruses in lepidopteran hosts that are mildly or non-permissive to virus- replication by: - Assessing the extent to which and the mechanisms whereby the immunosuppressive viruses, CiV and CsV or their genes enhance AcMNPV replication in polydnavirus- immunosuppressed H. zea and S. littoralis insects and S. littoralis cells. - Identifying CiV and CsV genes involved in the above immunosuppression (e.g. inhibiting cellular encapsulation and disrupting humoral immunity). This study will provide insight to the molecular mechanisms of viral pathogenesis and improve our understanding of insect immunity. This knowledge is of fundamental importance to controlling insect vectored diseases of humans, animals and plants and essential to developing novel means for pest control (including baculoviruses) that strategically weaken insect defenses to improve pathogen (i.e. biocontrol agent) infection and virulence.
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Cahaner, Avigdor, Susan J. Lamont, E. Dan Heller e Jossi Hillel. Molecular Genetic Dissection of Complex Immunocompetence Traits in Broilers. United States Department of Agriculture, agosto 2003. http://dx.doi.org/10.32747/2003.7586461.bard.
Testo completoAbstract (sommario):
Objectives: (1) Evaluate Immunocompetence-OTL-containing Chromosomal Regions (ICRs), marked by microsatellites or candidate genes, for magnitude of direct effect and for contribution to relationships among multiple immunocompetence, disease-resistance, and growth traits, in order to estimate epistatic and pleiotropic effects and to predict the potential breeding applications of such markers. (2) Evaluate the interaction of the ICRs with genetic backgrounds from multiple sources and of multiple levels of genetic variation, in order to predict the general applicability of molecular genetic markers across widely varied populations. Background: Diseases cause substantial economic losses to animal producers. Emerging pathogens, vaccine failures and intense management systems increase the impact of diseases on animal production. Moreover, zoonotic pathogens are a threat to human food safety when microbiological contamination of animal products occurs. Consumers are increasingly concerned about drug residues and antibiotic- resistant pathogens derived from animal products. The project used contemporary scientific technologies to investigate the genetics of chicken resistance to infectious disease. Genetic enhancement of the innate resistance of chicken populations provides a sustainable and ecologically sound approach to reduce microbial loads in agricultural populations. In turn, animals will be produced more efficiently with less need for drug treatment and will pose less of a potential food-safety hazard. Major achievements, conclusions and implications:. The PI and co-PIs had developed a refined research plan, aiming at the original but more focused objectives, that could be well-accomplished with the reduced awarded support. The successful conduct of that research over the past four years has yielded substantial new information about the genes and genetic markers that are associated with response to two important poultry pathogens, Salmonella enteritidis (SE) and Escherichia coli (EC), about variation of immunocompetence genes in poultry, about relationships of traits of immune response and production, and about interaction of genes with environment and with other genes and genetic background. The current BARD work has generated a base of knowledge and expertise regarding the genetic variation underlying the traits of immunocompetence and disease resistance. In addition, unique genetic resource populations of chickens have been established in the course of the current project, and they are essential for continued projects. The US laboratory has made considerable progress in studies of the genetics of resistance to SE. Microsatellite-marked chromosomal regions and several specific genes were linked to SE vaccine response or bacterial burden and the important phenomenon of gene interaction was identified in this system. In total, these studies demonstrate the role of genetics in SE response, the utility of the existing resource population, and the expertise of the research group in conducting such experiments. The Israeli laboratories had showed that the lines developed by selection for high or low level of antibody (Ab) response to EC differ similarly in Ab response to several other viral and bacterial pathogens, indicating the existence of a genetic control of general capacity of Ab response in young broilers. It was also found that the 10w-Ab line has developed, possibly via compensatory "natural" selection, higher cellular immune response. At the DNA levels, markers supposedly linked to immune response were identified, as well as SNP in the MHC, a candidate gene responsible for genetic differences in immunocompetence of chickens.
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Lamont, Susan J., E. Dan Heller e Avigdor Cahaner. Prediction of Immunocompetence and Resistance to Disease by Using Molecular Markers of the Major Histocompatibility Complex. United States Department of Agriculture, settembre 1994. http://dx.doi.org/10.32747/1994.7568780.bard.
Testo completoAbstract (sommario):
This project utilized two live-animal populations in an integrated research program to identify molecular markers for immune response and disease resistance. The populations each had their foundation from meat-type commercial breeder chicken lines of their respective countries. Investigations effectively used unique availability of resources in each country to study commercial-type environments in Israel and line-crosses with diverse inbred lines in the US. Two bacterial systems were investigated to cover both respiratory and gastrointestinal, and primary and secondary, infections. Individual experimental groups of animals were evaluated for combinations of vaccine antibody levels, response to pathogen challenge, growth parameters, genetic background and molecular markers. The positive association of antibody level with resistance to disease was confirmed. Effectiveness of genetic selection for vaccine antibody response level was demonstrated. Molecular markers, both inside and outside the MHC region, were associated with antibody response and resistance to disease. Markers were shown to have a generalized effect, by association with multiple traits of immune response and disease resistance. The impact of genetic background on marker effect was shown to be important. The overall results demonstrate the effectiveness of selection on vaccine antibody response and the potential of molecular marker-assisted selection to improve efficiency of production of meat-type chickens by reducing genetic susceptibility to disease.
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Lillehoj, Hyun, Dan Heller e Mark Jenkins. Cellular and molecular identification of Eimeria Acervulina Merozoite Antigens eliciting protective immunity. United States Department of Agriculture, novembre 1992. http://dx.doi.org/10.32747/1992.7561056.bard.
Testo completoAbstract (sommario):
Coccidiosis, ubiquitous diseases of poultry, seriously impair the growth and feed utilization of livestock and poultry. Coccidiosis causes over $600 million annual losses world-wide and no vaccine is currently available. The goal of this study was to investigate the cellular and molecular mechanisms controlling protective immune responses to coccidia parasites in order to develop immunological control strategy against coccidiosis. The major findings of this study were: 1) cell-mediated immunity plays a major role in protection against coccidiosis, 2) when different genetic lines showing different levels of disease susceptibility were compared, higher T-cell response was seen in the strains of chickens showing higher disease resistance, 3) early interferon secretion was observed in more coccidia-resistant chicken strains, 4) both sporozoite and merozoite antigens were able to induce interferon production, and 5) chicken monoclonal antibodies which detect immunogenic coccidia proteins have been developed. This study provided a good background work for future studies toward the development of recombinant coccidial vaccine. Availability of chicken monoclonal antibodies which detect immunogenic coccidia proteins will enhance our ability to identify potential coccidial vaccine antigens.
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Banai, Menachem, e Gary Splitter. Molecular Characterization and Function of Brucella Immunodominant Proteins. United States Department of Agriculture, luglio 1993. http://dx.doi.org/10.32747/1993.7568100.bard.
Testo completoAbstract (sommario):
The BARD project was a continuation of a previous BARD funded research project. It was aimed at characterization of the 12kDa immunodominant protein and subsequently the cloning and expression of the gene in E. coli. Additional immunodominant proteins were sought among genomic B. abortus expression library clones using T-lymphocyte proliferation assay as a screening method. The 12kDa protein was identified as the L7/L12 ribosomal protein demonstrating in the first time the role a structural protein may play in the development of the host's immunity against the organism. The gene was cloned from B. abortus (USA) and B. melitensis (Israel) showing identity of the oligonucleotide sequence between the two species. Further subcloning allowed expression of the protein in E. coli. While the native protein was shown to have DTH antigenicity its recombinant analog lacked this activity. In contrast the two proteins elicited lymphocyte proliferation in experimental murine brucellosis. CD4+ cells of the Th1 subset predominantly responded to this protein demonstrating the development of protective immunity (g-IFN, and IL-2) in the host. Similar results were obtained with bovine Brucella primed lymphocytes. UvrA, GroE1 and GroEs were additional Brucella immunodominant proteins that demonstrated MHC class II antigenicity. The role cytotoxic cells are playing in the clearance of brucella cells was shown using knock out mice defective either in their CD4+ or CD8+ cells. CD4+ defective mice were able to clear brucella as fast as did normal mice. In contrast mice which were defective in their CD8+ cells could not clear the organisms effectively proving the importance of this subtype cell line in development of protective immunity. The understanding of the host's immune response and the expansion of the panel of Brucella immunodominant proteins opened new avenues in vaccine design. It is now feasible to selectively use immunodominant proteins either as subunit vaccine to fortify immunity of older animals or as diagnostic reagents for the serological survaillance.
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Sessa, Guido, e Gregory B. Martin. molecular link from PAMP perception to a MAPK cascade associated with tomato disease resistance. United States Department of Agriculture, gennaio 2012. http://dx.doi.org/10.32747/2012.7597918.bard.
Testo completoAbstract (sommario):
The research problem: The detection of pathogen-associated molecular patterns (PAMPs) by plant pattern recognition receptors (PRRs) is a key mechanism by which plants activate an effective immune response against pathogen attack. MAPK cascades are important signaling components downstream of PRRs that transduce the PAMP signal to activate various defense responses. Preliminary experiments suggested that the receptor-like cytoplasmickinase (RLCK) Mai5 plays a positive role in pattern-triggered immunity (PTI) and interacts with the MAPKKK M3Kε. We thus hypothesized that Mai5, as other RLCKs, functions as a component PRR complexes and acts as a molecular link between PAMP perception and activation of MAPK cascades. Original goals: The central goal of this research was to investigate the molecular mechanisms by which Mai5 and M3Kε regulate plant immunity. Specific objectives were to: 1. Determine the spectrum of PAMPs whose perception is transmitted by M3Kε; 2. Identify plant proteins that act downstream of M3Kε to mediate PTI; 3. Investigate how and where Mai5 interacts with M3Kε in the plant cell; 4. Examine the mechanism by which Mai5 contributes to PTI. Changes in research directions: We did not find convincing evidence for the involvement of M3Kε in PTI signaling and substituted objectives 1 and 3 with research activities aimed at the analysis of transcriptomic profiles of tomato plants during the onset of plant immunity, isolation of the novel tomato PRR FLS3, and investigation of the involvement of the RLCKBSKs in PTI. Main achievements during this research program are in the following major areas: 1. Functional characterization of Mai5. The function of Mai5 in PTI signaling was demonstrated by testing the effect of silencing the Mai5 gene by virus-induced gene silencing (VIGS) experiments and in cell death assays. Domains of Mai5 that interact with MAPKKKs and subcellular localization of Mai5 were analyzed in detail. 2. Analysis of transcriptional profiles during the tomato immune responses to Pseudomonas syringae (Pombo et al., 2014). We identified tomato genes whose expression is induced specifically in PTI or in effector-triggered immunity (ETI). Thirty ETI-specific genes were examined by VIGS for their involvement in immunity and the MAPKKK EPK1, was found to be required for ETI. 3. Dissection of MAP kinase cascades downstream of M3Kε (Oh et al., 2013; Teper et al., 2015). We identified genes that encode positive (SGT and EDS1) and negative (WRKY1 and WRKY2) regulators of the ETI-associated cell death mediated by M3Kε. In addition, the MKK2 MAPKK, which acts downstream of M3Kε, was found to interact with the MPK3 MAPK and specific MPK3 amino acids involved interaction were identified and found to be required for induction of cell death. We also identified 5 type III effectors of the bacterial pathogen Xanthomonaseuvesicatoria that inhibited cell death induced by components of ETI-associated MAP kinase cascades. 4. Isolation of the tomato PRR FLS3 (Hind et al., submitted). FLS3, a novel PRR of the LRR-RLK family that specifically recognizes the flagellinepitope flgII-28 was isolated. FLS3 was shown to bind flgII-28, to require kinase activity for function, to act in concert with BAK1, and to enhance disease resistance to Pseudomonas syringae. 5. Functional analysis of RLCKs of the brassinosteroid signaling kinase (BSK) family.Arabidopsis and tomato BSKs were found to interact with PRRs. In addition, certain ArabidospsisBSK mutants were found to be impaired in PAMP-induced resistance to Pseudomonas syringae. Scientific and agricultural significance: Our research activities discovered and characterized new molecular components of signaling pathways mediating recognition of invading pathogens and activation of immune responses against them. Increased understanding of molecular mechanisms of immunity will allow them to be manipulated by both molecular breeding and genetic engineering to produce plants with enhanced natural defense against disease.
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Gafni, Yedidya, e Vitaly Citovsky. Inactivation of SGS3 as Molecular Basis for RNA Silencing Suppression by TYLCV V2. United States Department of Agriculture, novembre 2013. http://dx.doi.org/10.32747/2013.7593402.bard.
Testo completoAbstract (sommario):
The Israeli isolate of Tomato yellow leaf curl geminivirus(TYLCV-Is) is a major tomato pathogen, causing extensive crop losses in Israel and in the south-eastern U.S. Yet, little is known about the molecular mechanisms of its interaction with tomato cells. One of the most interesting aspects of such interaction is how the invading virus counteracts the RNA silencing response of the plant. In the former BARD project, we have shown that TYLCV-Is V2 protein is an RNA silencing suppressor, and that this suppression is carried out via the interaction of V2 with the SGS3 component of the plant RNA silencing machinery. This reported project was meant to use our data as a foundation to elucidate the molecular mechanism by which V2 affects the SGS3 activity. While this research is likely to have an important impact on our understanding of basic biology of virus-plant interactions and suppression of plant immunity, it also will have practical implications, helping to conceive novel strategies for crop resistance to TYLCV-Is. Our preliminary data in regard to V2 activities and our present knowledge of the SGS3 function suggest likely mechanisms for the inhibitory effect of V2 on SGS3. We have shown that V2 possess structural and functional hallmarks of an F-box protein, suggesting that it may target SGS3 for proteasomal degradation. SGS3 contains an RNA-binding domain and likely functions to protect the cleavage produces of the primary transcript for subsequent conversion to double-stranded forms; thus, V2 may simply block the RNA binding activity of SGS3. V2 may also employ a combination of these mechanisms. These and other possibilities were tested in this reported project.
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McElwain, Terry F., Eugene Pipano, Guy H. Palmer, Varda Shkap, Stephn A. Hines e Wendy C. Brown. Protection of Cattle against Babesiosis: Immunization against Babesia bovis with an Optimized RAP-1/Apical Complex Construct. United States Department of Agriculture, settembre 1999. http://dx.doi.org/10.32747/1999.7573063.bard.
Testo completoAbstract (sommario):
Previous research and current efforts at control of babesiosis fall short of meeting the needs of countries where the disease is endemic, such as Israel, as well as the needs of exporting countries and countries bordering on endemic areas, such as the U.S. Our long-term goal is to develop improved methods of immunization against bovine babesiosis based on an understanding of the molecular mechanisms of immune protection and parasite targets of a protective immune response. In our previous BARD project, we established the basis for focusing on rhoptry antigens as components of a subunit vaccine against bovine babesiosis, and for additional research to better characterize rhoptry associated protein-1 (RAP-1) as a target of protective immunity. In this continuation BARD project, our objectives were to [1] optimize the immune response against RAP-1, and [2] identify additional rhoptry candidate vaccine antigens. The entire locus encoding B. bovis RAP-1 was sequenced, and the rap-1 open reading frame compared among several strains. Unlike B. bigemina, in which multiple gene copies with variant domains encode RAP-1, the B. bovis RAP-1 locus contains only two identical genes which are conserved among strains. Through testing of multiple truncated constructs of rRAP-1, one or more immunodominant T cell epitopes were mapped to the amino terminal half of RAP-1. At least one linear and one conformational B cell epitope have been demonstrated in the same amino terminal construct, which in B. bigemina RAP-1 also contains an epitope recognized by neutralizing antibody. The amine terminal half of the molecule represents the most highly conserved part of the gene family and contains motifs conserved broadly among the apicomplexa. In contrast, the carboxy terminal half of B. bovis RAP-1 is less well conserved and contains multiple repeats encoding a linear B cell epitope potentially capable of inducing an ineffective, T cell independent, type 2 immune response. Therefore, we are testing an amino terminal fragment of RAP-1 (RAP-1N) in an immunization trial in cattle. Cattle have beer immunized with RAP-1N or control antigen, and IL-12 with Ribi adjuvant. Evaluation of the immune response is ongoing, and challenge with virulent B. bovis will occur in the near future. While no new rhoptry antigens were identified, our studies did identify and characterize a new spherical body antigen (SBP3), and several heat shock proteins (HSP's). The SBP3 and HSP21 antigens stimulate T cells from immune cattle and are considered new vaccine candidates worthy of further testing. Overall, we conclude that a single RAP-1 vaccine construct representing the conserved amino terminal region of the molecule should be sufficient for immunization against all strains of B. bovis. While results of the ongoing immunization trial will direct our next research steps, results at this time are consistent with our long term goal of designing a subunit vaccine which contains only the epitopes relevant to induction of protective immunity. Parallel studies are defining the mechanisms of protective immunity. Apicomplexan protozoa, including babesiosis and malaria, cause persistent diseases for which control is inadequate. The apical organelles are defining features of these complex protozoa, and have been conserved through the evolutionary process, Past and current BARD projects on babesiosis have established the validity and potential of exploiting these conserved organelles in developing improved control methods applicable to all apicomplexan diseases.
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Sessa, Guido, e Gregory Martin. role of FLS3 and BSK830 in pattern-triggered immunity in tomato. United States Department of Agriculture, gennaio 2016. http://dx.doi.org/10.32747/2016.7604270.bard.
Testo completoAbstract (sommario):
Pattern-recognition receptors (PRRs) located on the plant cell surface initiate immune responses by perceiving conserved pathogen molecules known as pathogen-associated molecular patterns (PAMPs). PRRs typically function in multiprotein complexes that include transmembrane and cytoplasmickinases and contribute to the initiation and signaling of pattern-triggered immunity (PTI). An important challenge is to identify molecular components of PRR complexes and downstream signaling pathways, and to understand the molecular mechanisms that mediate their function. In research activities supported by BARD-4931, we studied the role of the FLAGELLIN SENSING 3 (FLS3) PRR in the response of tomato leaves to flagellin-derivedPAMPs and PTI. In addition, we investigated molecular properties of the tomato brassinosteroid signaling kinase 830 (BSK830) that physically interacts with FLS3 and is a candidate for acting in the FLS3 signaling pathway. Our investigation refers to the proposal original objectives that were to: 1) Investigate the role of FLS3 and its interacting proteins in PTI; 2) Investigate the role of BSK830 in PTI; 3) Examine molecular and phosphorylation dynamics of the FLS3-BSK830 interaction; 4) Examine the possible interaction of FLS3 and BSK830 with Pstand Xcveffectors. We used CRISPR/Cas9 techniques to develop plants carrying single or combined mutations in the FLS3 gene and in the paralogsFLS2.1 and FLS2.2 genes, which encode the receptor FLAGELLIN SENSING2 (FLS2), and analyzed their function in PTI. Domain swapping analysis of the FLS2 and FLS3 receptors revealed domains of the proteins responsible for PAMP detection and for the different ROS response initiated by flgII-28/FLS3 as compared to flg22/FLS2. In addition, in vitro kinase assays and point mutations analysis identified FLS2 and FLS3 domains required for kinase activity and ATP binding. In research activities on tomato BSK830, we found that it interacts with PRRs and with the co-receptor SERK3A and PAMP treatment affects part of these interactions. CRISPR/Cas9 bsk830 mutant plants displayed enhanced pathogen susceptibility and reduced ROS production upon PAMP treatment. In addition, BSK830 interacted with 8 Xanthomonastype III secreted effectors. Follow up analysis revealed that among these effectors XopAE is part of an operon, is translocated into plant cells, and displays E3 ubiquitinligase activity. Our investigation was also extended to other Arabidopsis and tomato BSK family members. Arabidopsis BSK5 localized to the plant cell periphery, interacted with receptor-like kinases, and it was phosphorylatedin vitro by the PEPR1 and EFRPRRs. bsk5 mutant plants displayed enhanced susceptibility to pathogens and were impaired in several, but not all, PAMP-induced responses. Conversely, BSK5 overexpression conferred enhanced disease resistance and caused stronger PTI responses. Genetic complementation suggested that proper localization, kinase activity, and phosphorylation by PRRs are critical for BSK5 function. BSK7 and BSK8 specifically interacted with the FLS2 PRR, their respective mutant plants were more susceptible to B. cinereaand displayed reduced flg22-induced responses. The tomato BSK Mai1 was found to interact with the M3KMAPKKK, which is involved in activation of cell death associated with effector-triggered immunity. Silencing of Mai1 in N. benthamianaplants compromised cell death induced by a specific class of immune receptors. In addition, co-expression of Mai1 and M3Kin leaves enhanced MAPKphosphorylation and cell death, suggesting that Mai1 acts as a molecular link between pathogen recognition and MAPK signaling. Finally, We identified the PP2C phosphatase Pic1 that acts as a negative regulator of PTI by interacting with and dephosphorylating the receptor-like cytoplasmickinase Pti1, which is a positive regulator of plant immunity. The results of this investigation shed new light on the molecular characteristics and interactions of components of the immune system of crop plants providing new knowledge and tools for development of novel strategies for disease control.