Gotowe bibliografie tematyczne / Host Immune Respose

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Gotowa bibliografia na temat „Host Immune Respose”

Autor: Grafiati

Data publikacji: 6 września 2023

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Artykuły w czasopismach na temat "Host Immune Respose"

Hamadou, Takieddine, Imene Hamadou, Ahmed Menad, Somia Bouameur i Souad Ameddah. "COVID-19 : histoire, pathogenèse et réponse immunitaire de l'hôte". Batna Journal of Medical Sciences (BJMS) 8, nr 1 (4.06.2021): 52–58. http://dx.doi.org/10.48087/bjmsra.2021.8110.

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By the end of 2019, pneumonia of unknown etiology occurred in Wuhan, China. Local hospitals started receiving patients presenting symptoms like dry cough, fatigue, and breathing difficulties, most of these patients were linked to the Huanan seafood market, Wuhan, China. The pandemic was afterward confirmed to be associated with a novel coronavirus. The virus spread quickly from Wuhan to other provinces of China, then from china to the rest of the world causing thereby one of the most brutal pandemics in the world’s history. SARS-CoV2 has a long incubation period ranging from 3 to 7 days and can go up to 14 days in some cases which makes the infection difficult to be detected early and subsequently the disease spread harder to be controlled. SARS-CoV-2 is a single-stranded RNA virus with 4 main structural proteins, the spike (S) glycoprotein, the small envelope (E) the glycoprotein, the membrane (M) glycoprotein as well as the nucleocapsid (N) protein. Current knowledge about the virus shows that it uses its spike protein to invade host cells, mainly the alveolar epithelial cells. The the lung is the most targeted organ among many other organs like the heart, small intestine, and kidneys that are vulnerable to SARS-CoV-2 infection. The COVID-19 is known to be mild in most cases, but in some cases, it can be severe or even fatal. In the severe cases, acute respiratory distress syndrome was reported, and the the capability of SARS-CoV-2 to infect many organs can lead to multiorgan failure and death. SARS-CoV-2 invasion induces several immune responses that could be efficient for infection clearance in mild cases, while in severe cases, the immune response dysfunctions can even contribute to the disease aggravation. Neither the the pathogenic mechanism by which SARS-CoV-2 infects host cells, nor the host immune response to its infection have been fully understood, hence further studies are needed to give further evidence about these two phenomena. Keywords: COVID-19, SARS-CoV-2, Coronavirus, Structural proteins, Immune response.

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Haig, David M., Jackie Thomson, Colin McInnes, Catherine McCaughan, Wendy Imlach, Andrew Mercer i Stephen Fleming. "Orf virus immuno-modulation and the host immune response". Veterinary Immunology and Immunopathology 87, nr 3-4 (wrzesień 2002): 395–99. http://dx.doi.org/10.1016/s0165-2427(02)00087-9.

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Roilides, Emmanuel, Emmanuel Roilides, Maria Simitsopoulou, Aspasia Katragkou i Thomas J. Walsh. "Host immune response againstScedosporiumspecies". Medical Mycology 47, nr 4 (styczeń 2009): 433–40. http://dx.doi.org/10.1080/13693780902738006.

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Trasia, Reqgi First. "Host Immune Response to Malaria". International Islamic Medical Journal 2, nr 2 (28.07.2021): 67–71. http://dx.doi.org/10.33086/iimj.v2i2.1681.

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Malaria is still a health threat, especially for children and pregnant women in endemic areas. The World Health Organization (WHO) reports 228 million cases of malaria occur worldwide and an estimated 405,000 deaths from malaria globally in 2018. A series of malaria control efforts according to WHO recommendations have been carried out widely. However, these programs face obstacles. Therefore, the existence of an effective malaria vaccine is absolutely necessary in a series of malaria control strategies. Development of a malaria vaccine requires a basic concept regarding the host's immune response to malaria. Unfortunately, only a few in Indonesia have reviewed how the immune response is. This article will present an understanding of how the human immune system responds to Plasmodium falciparum.

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Cheng, E. "Imaging the Host Immune Response". Science Translational Medicine 2, nr 40 (13.07.2010): 40ec113. http://dx.doi.org/10.1126/scitranslmed.3001469.

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Li, Chaozheng, Shaoping Weng i Jianguo He. "WSSV–host interaction: Host response and immune evasion". Fish & Shellfish Immunology 84 (styczeń 2019): 558–71. http://dx.doi.org/10.1016/j.fsi.2018.10.043.

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Bhopale, Mahendra. "Experimental Hookworm Infection in Laboratory animals: Parasite behavior, Immune response and Chemotherapeutic Studies". Biotechnology and Bioprocessing 2, nr 5 (24.06.2021): 01–03. http://dx.doi.org/10.31579/2766-2314/040.

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Hookworm disease is known to be caused allergic manifestation and severe anemic pathogenicity in man and canine hosts. Attempts have been made to establish laboratory models of Necator americaus, Ancylostoma duodenale, and Ancylostoma ceylanicum, together with canine parasite, Ancylostoma caninum. The studies include pathophysiological aspects of the host-parasite relationship, and develop to establish patent infection. Immunological approach to selecting antigen for diagnosis and protective immunity purpose using larval and adult worm antigens and their secretions became the focus with the subsequent discovery of cloning in vaccine development as main research interest. Chemotherapy of newer drug screening in laboratory models ultimately selected to use for preventive chemotherapy in hookworm endemic areas using recommended drugs.

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Jamieson, Amanda Mercedes, Meredith Crane, Yun Xu i Kayla Lee. "Immune triage: prioritization of host immune responses." Journal of Immunology 196, nr 1_Supplement (1.05.2016): 197.20. http://dx.doi.org/10.4049/jimmunol.196.supp.197.20.

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Abstract The immune response is important in many functions, including host defense against pathogens, wound healing, development, response to cancer, and maintenance of homeostatic physiological responses. We are interested in the concept of immune triage, in that a given host must be able to deal effectively with multiple insults, and at times prioritize immune responses. It is important for the overall health status of the host that the immune system responds effectively to protect essential organs. We have developed several mouse models, focusing on the lung immune response, that allow us to examine different aspects of immune triage. The lung is an essential and delicate organ and thus pulmonary immune responses must be tightly regulated. We have determined that lung infection with influenza A virus (IAV) alters the response to bacterial lung infections. Depending on the bacterial infection, previous infection with IAV can suppress or augment the immune response to bacteria. We have also determined that pulmonary infection with IAV alters many aspects of the systemic immune response. There is a global suppression to systemic bacterial infection, and a decrease in the wound healing response. Our data indicate that the immune system prioritizes lung infections over many other responses. This is most likely due to the importance of the lung in host survival. We have established several regulatory mechanisms by which this immune triage occurs. By understanding how the immune system responds to multiple insults we can improve our understanding of the immune network on a global level.

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Elaskandrany, Miar, Rohin Patel, Mintoo Patel, George Miller, Deepak Saxena i Anjana Saxena. "Fungi, host immune response, and tumorigenesis". American Journal of Physiology-Gastrointestinal and Liver Physiology 321, nr 2 (1.08.2021): G213—G222. http://dx.doi.org/10.1152/ajpgi.00025.2021.

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Advances in -omics analyses have tremendously enhanced our understanding of the role of the microbiome in human health and disease. Most research is focused on the bacteriome, but scientists have now realized the significance of the virome and microbial dysbiosis as well, particularly in noninfectious diseases such as cancer. In this review, we summarize the role of mycobiome in tumorigenesis, with a dismal prognosis, and attention to pancreatic ductal adenocarcinoma (PDAC). We also discuss bacterial and mycobial interactions to the host’s immune response that is prevalently responsible for resistance to cancer therapy, including immunotherapy. We reported that the Malassezia species associated with scalp and skin infections, colonize in human PDAC tumors and accelerate tumorigenesis via activating the C3 complement-mannose-binding lectin (MBL) pathway. PDAC tumors thrive in an immunosuppressive microenvironment with desmoplastic stroma and a dysbiotic microbiome. Host-microbiome interactions in the tumor milieu pose a significant threat in driving the indolent immune behavior of the tumor. Microbial intervention in multimodal cancer therapy is a promising novel approach to modify an immunotolerant (“cold”) tumor microenvironment to an immunocompetent (“hot”) milieu that is effective in eliminating tumorigenesis.

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Visser, Douwe H., Regan S. Solomons, Katharina Ronacher, Gijs T. van Well, Martijn W. Heymans, Gerhard Walzl, Novel N. Chegou, Johan F. Schoeman i Anne M. van Furth. "Host Immune Response to Tuberculous Meningitis". Clinical Infectious Diseases 60, nr 2 (9.10.2014): 177–87. http://dx.doi.org/10.1093/cid/ciu781.

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Rozprawy doktorskie na temat "Host Immune Respose"

Millhouse, Emma. "Microbial biofilm composition influences the host immune response". Thesis, University of Glasgow, 2015. http://theses.gla.ac.uk/6848/.

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Periodontal disease (PD) is a multifactorial disease of the oral cavity affecting the majority of the population. Although not a direct cause of mortality, PD is a health concern because it affects the majority of the population and has a negative impact on oral health, ability to chew, appearance, quality of life, dental care costs and can lead to tooth loss. Dental plaque is a microbial biofilm, which is necessary but not sufficient for the development of periodontitis. The interactions between the biofilm and the host cells, both local tissue and immune cells, can lead to tissue destruction and ultimately tooth loss. Clinical management of periodontitis involves mechanical removal of plaque from the tooth surface. Treatment is time consuming, in some patients only partially successful and recurrence is common. Therefore, understanding how the host interacts with microbial biofilms in both health and PD will help improve treatments and identify novel targets for therapeutic and preventative strategies. The hypothesis of this thesis is that the bacterial composition of oral biofilms may modulate host cell responses which contribute to the pathogenicity of PD. The overarching aim of this research was to develop an in vitro co-culture model system to study how biofilm composition can influence the host immune response. The studies document the development of health-associated, intermediate and disease-associated biofilms with host tissue and immune cells, and the use of these models to test antimicrobial and anti-inflammatory compounds as potential treatments for PD. The biofilms developed were assessed for survival in cell culture conditions and batch reproducibility by PCR and morphology visualised using SEM. The health-associated biofilm included Streptococcus mitis, S. intermedius and S. oralis (3-species); the intermediate biofilm additionally included Veillonella dispar, Actinomyces naeslundii, Fusobacterium nucleatum and F. nucleatum spp. Vincentii (7-species); and the disease-associated biofilm included further addition of Porphyromonas gingivalis, Prevotella intermedia, and Aggregatibacter actinomycetemcomitans (10-species). These biofilms were co-cultured with an oral epithelial cell line and primary gingival epithelial cells, as well as neutrophils and a myeloid cell line. Host cell viability was assessed by AlamarBlue®/LDH and changes in mRNA and protein expression of chemokines and cytokines were assessed by quantitative PCR and ELISA/Luminex®, respectively. Cellular responses were further evaluated by microscopy and flow cytometry. Generally, co-culture of health associated biofilms with host cells resulted in minimal impact on cell viability and generally low inflammatory gene expression and protein release, with some genes including CXCL5 and CCL1 being downregulated compared to the cells only control. Intermediate biofilms caused some cell death and a marked upregulation of inflammatory genes and protein release, including a 302.7 fold increase of epithelial cell IL-8 gene expression compared to the cells only control. These intermediate biofilms elicited significant upregulation of CD40 and CD69 expression on the monocyte cell line compared with untreated controls. Co-culture of the 10 species disease associated biofilms with host cells resulted in significant host cell death of both epithelial cells and monocytes. The 10 species biofilm caused significantly increased pro-inflammatory gene expression, but only low levels of protein could be detected in the supernatants. Similar trends in upregulation of inflammatory gene expression but low levels of protein release was observed in co-culture with differentiated pro-monocytes, whereas upregulation of inflammatory gene expression and protein release in neutrophil co-cultures was observed. The effect of antimicrobial and anti-inflammatory compounds, resveratrol and chlorhexidine, was evaluated using this model system. Prior treatment of epithelial cells with resveratrol and biofilm with chlorhexidine significantly reduced IL-8 release from epithelial cells in co-culture with biofilms for 4 and 24 hours. In conclusion, this research has developed and validated 3 complex multi-species biofilms to study host: biofilm interactions in vitro. Furthermore, using these models in co-culture with multiple host cell types, clear differences in the host response to different biofilms were observed. The variations in inflammatory response of host cells and oral biofilms observed in this study help further understanding of the complex host: biofilm interactions within the oral cavity which contribute to PD. This model demonstrated its potential as a platform to test novel actives, highlighting its use a tool to study how actives can influence host: biofilm interactions within the oral cavity. Future use of this model will aid in greater understanding of host: biofilm interactions. Such findings are applicable to oral health and beyond, and may help to identify novel therapeutic targets for the treatment of PD and other biofilm associated diseases.

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Tattermusch, Sonja. "The host immune response to HTLV-1 infection". Thesis, Imperial College London, 2012. http://hdl.handle.net/10044/1/9916.

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Human T-lymphotropic virus Type 1 (HTLV-1) is a retrovirus that persists lifelong in the host. In ~4% of infected people, HTLV-1 causes a chronic disabling neuroinflammatory disease known as HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). The pathogenesis of HAM/TSP is unknown and treatment remains ineffective. In this study we aimed to identify patterns in frequencies of peripheral leukocyte populations and blood gene expression profiles of HTLV-1 carriers that suggest new hypotheses as to the mechanisms of HTLV-1 persistence and HAM/TSP pathology. Flow cytometric immunophenotyping of peripheral blood leukocytes revealed abnormal activation and maturation profiles of effector T cells but not antigen-presenting cells. High frequencies of circulating granzyme and perforin-rich CD8+ T cells were associated with an increased probability of HAM/TSP. However, the cytolytic capacity of these T cells is not known as although they accumulated cytolytic proteins, granzyme mRNA levels were down-regulated in patients with HAM/TSP. Furthermore, presence of HAM/TSP was associated with an expansion of CD56-negative NK cells, which are thought to have decreased cytolytic functions. Blood gene expression profiles identified perturbations of the p53 signalling pathway as a hallmark of HTLV-1 infection. In contrast, a subset of interferon (IFN)-stimulated genes was over-expressed in patients with HAM/TSP but not in asymptomatic HTLV-1 carriers or patients with the clinically similar disease multiple sclerosis. The IFN-inducible signature was present in all circulating leukocytes and its intensity correlated with the clinical severity of HAM/TSP. Leukocytes from patients with HAM/TSP were primed to respond strongly to stimulation with exogenous IFN. However, while type I IFN suppressed expression of the HTLV-1 structural protein Gag it failed to suppress the highly immunogenic viral transcriptional transactivator Tax. Based on our findings we hypothesise that impaired NK cell and T cell-mediated immune responses result in high HTLV-1 proviral loads but that the over-expression of a subset of IFN-stimulated genes contributes to the development of HAM/TSP.

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Verma, Meghna. "Modeling Host Immune Responses in Infectious Diseases". Diss., Virginia Tech, 2019. http://hdl.handle.net/10919/96019.

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Infectious diseases caused by bacteria, fungi, viruses and parasites have affected humans historically. Infectious diseases remain a major cause of premature death and a public health concern globally with increased mortality and significant economic burden. Unvaccinated individuals, people with suppressed and compromised immune systems are at higher risk of suffering from infectious diseases. In spite of significant advancements in infectious diseases research, the control or treatment process faces challenges. The mucosal immune system plays a crucial role in safeguarding the body from harmful pathogens, while being constantly exposed to the environment. To develop treatment options for infectious diseases, it is vital to understand the immune responses that occur during infection. The two infectious diseases presented here are: i) Helicobacter pylori infection and ii) human immunodeficiency (HIV) and human papillomavirus (HPV) co-infection. H pylori, is a bacterium that colonizes the stomach and causes gastric cancer in 1-2% but is beneficial for protection against allergies and gastroesophageal diseases. An estimated 85% of H pylori colonized individuals show no detrimental effects. HIV is a virus that causes AIDS, one of the deadliest and most persistent epidemics. HIV-infected patients are at an increased risk of co-infection with HPV, and report an increased incidence of oral cancer. The goal of this thesis is to elucidate the host immune responses in infectious diseases via the use of computational and mathematical models. First, the thesis reviews the need for computational and mathematical models to study the immune responses in the course of infectious diseases. Second, it presents a novel sensitivity analysis method that identifies important parameters in a hybrid (agent-based/equation-based) model of H. pylori infection. Third, it introduces a novel model representing the HIV/HPV coinfection and compares the simulation results with a clinical study. Fourth, it discusses the need of advanced modeling technologies to achieve a personalized systems wide approach and the challenges that can be encountered in the process. Taken together, the work in this dissertation presents modeling approaches that could lead to the identification of host immune factors in infectious diseases in a predictive and more resource-efficient manner.
Doctor of Philosophy
Infectious diseases caused by bacteria, fungi, viruses and parasites have affected humans historically. Infectious diseases remain a major cause of premature death and a public health concern globally with increased mortality and significant economic burden. These infections can occur either via air, travel to at-risk places, direct person-to-person contact with an infected individual or through water or fecal route. Unvaccinated individuals, individuals with suppressed and compromised immune system such as that in HIV carriers are at higher risk of getting infectious diseases. In spite of significant advancements in infectious diseases research, the control and treatment of these diseases faces numerous challenges. The mucosal immune system plays a crucial role in safeguarding the body from harmful pathogens, while being exposed to the environment, mainly food antigens. To develop treatment options for infectious diseases, it is vital to understand the immune responses that occur during infection. In this work, we focus on gut immune system that acts like an ecosystem comprising of trillions of interacting cells and molecules, including membars of the microbiome. The goal of this dissertation is to develop computational models that can simulate host immune responses in two infectious diseases- i) Helicobacter pylori infection and ii) human immunodeficiency virus (HIV)-human papilloma virus (HPV) co-infection. Firstly, it reviews the various mathematical techniques and systems biology based methods. Second, it introduces a "hybrid" model that combines different mathematical and statistical approaches to study H. pylori infection. Third, it highlights the development of a novel HIV/HPV coinfection model and compares the results from a clinical trial study. Fourth, it discusses the challenges that can be encountered in adapting machine learning based computational technologies. Taken together, the work in this dissertation presents modeling approaches that could lead to the identification of host immune factors in infectious diseases in a predictive and more resourceful way.

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Watret, Karen Christine. "Graft-versus-host reaction and the mucosal immune response". Thesis, University of Edinburgh, 1990. http://hdl.handle.net/1842/19395.

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Post, Frank A. "Mycobacterial strain diversity : impact on the host immune response". Doctoral thesis, University of Cape Town, 2003. http://hdl.handle.net/11427/2717.

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Rowland, Caroline A. "Characterisation of host immune responses to Burkholderia mallei". Thesis, Open University, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.439229.

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Anderson, J. J. "The immune response to respiratory syncytial virus in an animal model". Thesis, University of Newcastle Upon Tyne, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.380769.

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Smith, A. L. "Immunity response to Eimeria vermiformis infection in the mouse". Thesis, University of Nottingham, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.284111.

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Parsa, Venkata Laxmi Kishore. "Molecular mechanisms of host cell response to Francisella infection". Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1195584597.

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Ringqvist, Emma. "Host-Pathogen Responses during Giardia infections". Doctoral thesis, Uppsala universitet, Mikrobiologi, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-108980.

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Giardia lamblia is a eukaryotic parasite of the upper small intestine of humans and animals. The infecting trophozoite cells do not invade the epithelium lining of the intestine, but attach to the brush border surface in the intestinal lumen. The giardiasis disease in humans is highly variable. Prior to this study, the molecular mechanisms involved in establishment of infection or cause of disease were largely uncharacterized. In this thesis, the molecular relationship between Giardia and the human host is described. The interaction of the parasite with human epithelial cells was investigated in vitro. Changes in the transcriptome and proteome of the parasite and the host cells, and changes in the micro-environment of the infection have been identified using microarray technology, and 1- and 2-Dimensional SDS-PAGE protein mapping together with mass spectrometry identification. The first large-scale description of cellular activities within host epithelial cells during Giardia infection is included in this thesis (Paper I). We identified a unique activation of the host immune response and induction of apoptosis upon infection by Giardia. Four important virulence factors of the parasite, directly linked to the success of Giardia infection, were characterized and are presented in Papers II and III. The parasite was shown to have immune-modulating capacities, and to release proteins during host-interaction that facilitate the establishment of infection. Additional putative virulence factors were found among Giardia genes transcriptionally up-regulated during early infection (Paper IV). In summary, this thesis provides important insights into the molecular mechanisms of the host-parasite interaction.

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Książki na temat "Host Immune Respose"

PhD, Henderson Brian, i Oyston Petra C. F, red. Bacterial evasion of host immune responses. Cambridge, UK: Cambridge University Press, 2003.

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Shigeyuki, Hamada, Holt Stanley C i McGhee Jerry R, red. Periodontal disease: Pathogens & host immune responses. Tokyo: Quintessence Pub., 1991.

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W, Murphy Juneann, Friedman Herman 1931- i Bendinelli Mauro, red. Fungal infections and immune responses. New York: Plenum Press, 1993.

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H, Koszinowski U., i Hengel H, red. Viral proteins counteracting host defenses. Berlin: Springer, 2002.

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The immune response to infection. Washington, DC: ASM Press, 2011.

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Venketaraman, Vishwanath, red. Understanding the Host Immune Response Against Mycobacterium tuberculosis Infection. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-97367-8.

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W, Ades Edwin, Morse Stephen A i Rest Richard F, red. Microbial pathogenesis and immune response II. New York: New York Academy of Sciences, 1996.

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Diamond, Michael S. West Nile encephalitis virus infection: Viral pathogenesis and the host immune response. New York, NY: Springer, 2009.

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S, Diamond Michael, red. West Nile encephalitis virus infection: Viral pathogenesis and the host immune response. New York: Springer, 2008.

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J, Brown Stephen. Host immune response to feeding by ticks: A natural biological control mechanism. Nairobi, Kenya: ICIPE Science Press, International Centre of Insect Physiology and Ecology, 1988.

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Części książek na temat "Host Immune Respose"

Holland, Steven M. "Genetics of Antibacterial Host Defenses". W The Immune Response to Infection, 471–82. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555816872.ch37.

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Madera, Laurence, Shuhua Ma i Robert E. W. Hancock. "Host Defense (Antimicrobial) Peptides and Proteins". W The Immune Response to Infection, 57–67. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555816872.ch4.

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Tischler, Anna D., i John D. McKinney. "Bacterial Strategies for Survival in the Host". W The Immune Response to Infection, 425–40. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555816872.ch34.

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Blackwell, Jenefer M. "Immunogenetics of Host Response to Parasites in Humans". W The Immune Response to Infection, 483–90. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555816872.ch38.

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Gregory, Meredith, Michelle C. Callegan i Michael S. Gilmore. "Role of Bacterial and Host Factors in Infectious Endophthalmitis". W Immune Response and the Eye, 266–75. Basel: KARGER, 2007. http://dx.doi.org/10.1159/000099277.

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Corbeil, Lynette B. "Host Immune Response to Histophilus somni". W Current Topics in Microbiology and Immunology, 109–29. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/82_2015_5012.

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Al-Harrasi, Ahmed, Saurabh Bhatia, Tapan Behl i Deepak Kaushik. "Host Immune Response vs. COVID-19". W Role of Essential Oils in the Management of COVID-19, 99–107. Boca Raton: CRC Press, 2022. http://dx.doi.org/10.1201/9781003175933-7.

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Yoshinaga, Masao, Koichiro Miyata i Vincent A. Fischetti. "Human Secretory Immune Response to Streptococcal M Protein". W Streptococci and the Host, 913–15. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4899-1825-3_213.

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Kozel, T. R. "Suppression of Host Resistance by Antigens of Cryptococcus Neoformans". W Fungal Cell Wall and Immune Response, 399–413. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76074-7_30.

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Dhesi, Zaneeta, Susanne Herbst i Darius Armstrong-James. "Transcript Profiling of the Murine Immune Response to Invasive Aspergillosis". W Host-Fungus Interactions, 435–44. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-539-8_30.

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Streszczenia konferencji na temat "Host Immune Respose"

Kobayashi, Hisataka. "Near infrared photoimmunotherapy rapidly elicits specific host immunity against cancer cells (Conference Presentation)". W Biophotonics and Immune Responses XII, redaktor Wei R. Chen. SPIE, 2017. http://dx.doi.org/10.1117/12.2249943.

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Lee, Bok-Luel. "Host immune responses inRiptortus-Burkholderiagut symbiotic system". W 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.90799.

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Smilanich, Angela. "Host range expansion and the insect immune response". W 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.93627.

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Flerlage, T., E. K. Allen, A. Zamora, J. Crawford i P. G. Thomas. "Host Immune Response in Pediatric Acute Respiratory Distress Syndrome". W American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a7253.

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Segal, Leopoldo, Rohan Kulkarni, William Rom i Michael Weiden. "Assessment Of Lung Microbiomeand Host Immune Response In Emphysema". W American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a1440.

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Gautam, Avinita, i Anupam Priyadarshi. "Mathematical modelling of Toxoplasma Gondii and host immune response". W PROCEEDINGS OF THE INTERNATIONAL CONFERENCE ON FRONTIERS IN INDUSTRIAL AND APPLIED MATHEMATICS (FIAM-2018). Author(s), 2018. http://dx.doi.org/10.1063/1.5042172.

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Huang, Yong, Shwu-Fan Ma, Rekha Vij, Justin Oldham, Gary Huffnagle, John Erb-Downward, Kevin Flaherty i in. "Microbes mediated host innate immune response in idiopathic pulmonary fibrosis". W ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa881.

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Gollnick, Sandra O., Edith Kabingu, Philaretos C. Kousis i Barbara W. Henderson. "Stimulation of the host immune response by photodynamic therapy (PDT)". W Biomedical Optics 2004, redaktorzy Steven L. Jacques i William P. Roach. SPIE, 2004. http://dx.doi.org/10.1117/12.530437.

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Imoto, Shigeru, Noriko Nakatsugawa, Hirotsugu Isaka, Hiroki Ito, Kentaro Imi, Kaisuke Miyamoto i Tetsuya Nakatsura. "Abstract 450: Host-tumor immune response for breast cancer patients." W Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-450.

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Kamareddine, Layla, Hoda Najjar, Abeer Mohbeddin, Nawar Haj Ahmed i Paula Watnick. "Between Immunity, Metabolism, and Development: A story of a Fly Gut!" W Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0141.

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In addition to its role in initiating immune response in the body, the innate immune system seems to also play a critical role in maintaining homeostatic balance in the gut epithelium. Our recent studies in the Drosophila melanogaster fruit fly model suggest that different innate immune pathways contribute to this homeostatic balance through activating the transcription of genes encoding antimicrobial peptides. We provide evidence that several metabolic parameters are altered in immune deficient flies. We also highlight a role of the gut flora, particularly through its short chain fatty acid, in contributing to this metabolic balance. Interestingly, our data suggest that impaired immunity and metabolic alteration, in turn, exhibit an effect on host development. Collectively, these findings provide evidence that innate immune pathways not only provide the first line of defense against infection but also contribute to host metabolism and development.

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Raporty organizacyjne na temat "Host Immune Respose"

Nataro, James P., i David K. Karaolis. Host Immune Response to Bacterial Cyclic Diguanylic Acid (c-di-GMP). Fort Belvoir, VA: Defense Technical Information Center, lipiec 2009. http://dx.doi.org/10.21236/ada533324.

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Chejanovsky, Nor, i Bruce A. Webb. Potentiation of Pest Control by Insect Immunosuppression. United States Department of Agriculture, styczeń 2010. http://dx.doi.org/10.32747/2010.7592113.bard.

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The restricted host range of many baculoviruses, highly pathogenic to Lepidoptera and non-pathogenic to mammals, limits their use to single or few closely related Lepidopteran species and is an obstacle to extending their implementation for pest control. The insect immune response is a major determinant of the ability of an insect pathogen to efficiently multiply and propagate. We have developed an original model system to study the Lepidopteran antiviral immune response based on Spodoptera littoralis resistance to AcMNPV (Autographa californica multiple nucleopolyhedrovirus) infection and the fascinating immunosuppressive activity of polydnaviruses .Our aim is to elucidate the mechanisms through which the immunosuppressive insect polydnaviruses promote replication of pathogenic baculoviruses in lepidopteran hosts that are mildly or non-permissive to virus- replication. In this study we : 1- Assessed the extent to which and the mechanisms whereby the immunosuppressive Campoletis sonorensis polydnavirus (CsV) or its genes enhanced replication of a well-characterized pathogenic baculovirus AcMNPV, in polydnavirus-immunosuppressedH. zea and S. littoralis insects and S. littoralis cells, hosts that are mildly or non-permissive to AcMNPV. 2- Identified CsV genes involved in the above immunosuppression (e.g. inhibiting cellular encapsulation and disrupting humoral immunity). We showed 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, the baculovirus AcMNPV, to infect the pest. 3. For the first time two PDV-specific genes of the vankyrin and cystein rich-motif families involved in immunosuppression of the host, namely Pvank1 and Hv1.1 respectively, enhanced the efficacy of an insect pathogen toward a semipermissive pest. 4. Pvank1 inhibits apoptosis of Spodopteran cells elucidating one functional aspect of PDVvankyrins. 5. That Pvank-1 and Hv1.1 do not show cooperative effect in S. littoralis when co-expressed during AcMNPV infection. Our results pave the way to developing novel means for pest control, including baculoviruses, that rely upon suppressing host immune systems by strategically weakening insect defenses to improve pathogen (i.e. biocontrol agent) infection and virulence. Also, we expect that the above result will help to develop systems for enhanced insect control that may ultimately help to reduce transmission of insect vectored diseases of humans, animals and plants as well as provide mechanisms for suppression of insect populations that damage crop plants by direct feeding.

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Evans, Donald L., Avigdor Eldar, Liliana Jaso-Friedmann i Herve Bercovier. Streptococcus Iniae Infection in Trout and Tilapia: Host-Pathogen Interactions, the Immune Response Towards the Pathogen and Vaccine Formulation. United States Department of Agriculture, luty 2005. http://dx.doi.org/10.32747/2005.7586538.bard.

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The objectives of the BARD proposal were to determine the mechanisms of nonspecific cytotoxic cells (NCC) that are necessary to provide heightened innate resistance to infection and to identify the antigenic determinants in Streptococcus iniae that are best suited for vaccine development. Our central hypothesis was that anti-bacterial immunity in trout and tilapia can only be acquired by combining "innate" NCC responses with antibody responses to polysaccharide antigens. These Objectives were accomplished by experiments delineated by the following Specific Aims: Specific aim (SA) #1 (USA) "Clone and Identify the Apoptosis Regulatory Genes in NCC"; Specific aim #2 (USA)"Identify Regulatory Factors that Control NCC Responses to S. iniae"; Specific aim #3 (Israel) "Characterize the Biological Properties of the S. iniae Capsular Polysaccharide"; and Specific aim #4 (Israel) "Development of an Acellular Vaccine". Our model of S. iniae pathogenesis encompassed two approaches, identify apoptosis regulatory genes and proteins in tilapia that affected NCC activities (USA group) and determine the participation of S.iniae capsular polysaccharides as potential immunogens for the development of an acellular vaccine (Israel group). We previously established that it was possible to immunize tilapia and trout against experimental S. difficile/iniaeinfections. However these studies indicated that antibody responses in protected fish were short lived (3-4 months). Thus available vaccines were useful for short-term protection only. To address the issues of regulation of pathogenesis and immunogens of S. iniae, we have emphasized the role of the innate immune response regarding activation of NCC and mechanisms of invasiveness. Considerable progress was made toward accomplishing SA #1. We have cloned the cDNA of the following tilapia genes: cellular apoptosis susceptibility (CAS/AF547173»; tumor necrosis factor alpha (TNF / A Y 428948); and nascent polypeptide-associated complex alpha polypeptide (NACA/ A Y168640). Similar attempts were made to sequence the tilapia FasLgene/cDNA, however these experiments were not successful. Aim #2 was to "Identify Regulatory Factors that Control NCC Responses to S. iniae." To accomplish this, a new membrane receptor has been identified that may control innate responses (including apoptosis) of NCC to S. iniae. The receptor is a membrane protein on teleost NCC. This protein (NCC cationic antimicrobial protein-1/ncamp-1/AAQ99138) has been sequenced and the cDNA cloned (A Y324398). In recombinant form, ncamp-l kills S. iniae in vitro. Specific aim 3 ("Characterize the Biological Properties of the S.iniae Capsular Polysaccharide") utilized an in- vitro model using rainbow trout primary skin epithelial cell mono layers. These experiments demonstrated colonization into epithelial cells followed by a rapid decline of viable intracellular bacteria and translocation out of the cell. This pathogenesis model suggested that the bacterium escapes the endosome and translocates through the rainbow trout skin barrier to further invade and infect the host. Specific aim #4 ("Development of an Acellular Vaccine") was not specifically addressed. These studies demonstrated that several different apoptotic regulatory genes/proteins are expressed by tilapia NCC. These are the first studies demonstrating that such factors exist in tilapia. Because tilapia NCC bind to and are activated by S. iniae bacterial DNA, we predict that the apoptotic regulatory activity of S. iniae previously demonstrated by our group may be associated with innate antibacterial responses in tilapia.

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Eldar, Avigdor, i 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, grudzień 2000. http://dx.doi.org/10.32747/2000.7575286.bard.

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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, i Bruce A. Webb. Potentiation of pest control by insect immunosuppression. United States Department of Agriculture, lipiec 2004. http://dx.doi.org/10.32747/2004.7587236.bard.

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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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Chejanovsky, Nor, Diana Cox-Foster, Victoria Soroker i Ron Ophir. Honeybee modulation of infection with the Israeli acute paralysis virus, in asymptomatic, acutely infected and CCD colonies. United States Department of Agriculture, grudzień 2013. http://dx.doi.org/10.32747/2013.7594392.bard.

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Honey bee (Apis mellifera) colony losses pose a severe risk to the food chain. The IAPV (Israeli acute paralysis virus) was correlated with CCD, a particular case of colony collapse. Honey bees severely infected with IAPV show shivering wings that progress to paralysis and subsequent death. Bee viruses, including IAPV, are widely present in honey bee colonies but often there are no pathological symptoms. Infestation of the beehive with Varroa mites or exposure to stress factors leads to significant increase in viral titers and fatal infections. We hypothesized that the honey bee is regulating/controlling IAPV and viral infections in asymptomatic infections and this control is broken through "stress" leading to acute infections and/or CCD. Our aims were: 1. To discover genetic changes in IAPV that may affect tissue tropism in the host, and/or virus infectivity and pathogenicity. 2. To elucidate mechanisms used by the host to regulate/ manage the IAPV-infection in vivo and in vitro. To achieve the above objectives we first studied stress-induced virus activation. Our data indicated that some pesticides, including myclobutanil, chlorothalonil and fluvalinate, result in amplified viral titers when bees are exposed at sub lethal levels by a single feeding. Analysis of the level of immune-related bee genes indicated that CCD-colonies exhibit altered and weaker immune responses than healthy colonies. Given the important role of viral RNA interference (RNAi) in combating viral infections we investigated if CCD-colonies were able to elicit this particular antiviral response. Deep-sequencing analysis of samples from CCD-colonies from US and Israel revealed high frequency of small interfering RNAs (siRNA) perfectly matching IAPV, Kashmir bee virus and Deformed wing virus genomes. Israeli colonies showed high titers of IAPV and a conserved RNAi pattern of targeting the viral genome .Our findings were further supported by analysis of samples from colonies experimentally infected with IAPV. Following for the first time the dynamics of IAPV infection in a group of CCD colonies that we rescued from collapse, we found that IAPV conserves its potential to act as one lethal, infectious factor and that its continuous replication in CCD colonies deeply affects their health and survival. Ours is the first report on the dominant role of IAPV in CCD-colonies outside from the US under natural conditions. We concluded that CCD-colonies do exhibit a regular siRNA response that is specific against predominant viruses associated with colony losses and other immune pathways may account for their weak immune response towards virus infection. Our findings: 1. Reveal that preventive measures should be taken by the beekeepers to avoid insecticide-based stress induction of viral infections as well as to manage CCD colonies as a source of highly infectious viruses such as IAPV. 2. Contribute to identify honey bee mechanisms involved in managing viral infections.

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Fast, L. D., C. R. Valeri i J. P. Crowley. Immune Responses to MHC Homozygous Lymphoid Cells in Murine F1 Hybrid Recipients: Implications for Transfusion Associated Graft-Versus Host Disease. Fort Belvoir, VA: Defense Technical Information Center, czerwiec 1994. http://dx.doi.org/10.21236/ada360361.

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Gafni, Yedidya, Moshe Lapidot i Vitaly Citovsky. Dual role of the TYLCV protein V2 in suppressing the host plant defense. United States Department of Agriculture, styczeń 2013. http://dx.doi.org/10.32747/2013.7597935.bard.

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TYLCV-Is is a major tomato pathogen, causing extensive crop losses in Israel and the U.S. We have identified a TYLCV-Is protein, V2, which acts as a suppressor of RNA silencing. Intriguingly, the counter-defense function of V2 may not be limited to silencing suppression. Our recent data suggest that V2 interacts with the tomato CYP1 protease. CYP1 belongs to the family of papain-like cysteine proteases which participate in programmed cell death (PCD) involved in plant defense against pathogens. Based on these data we proposed a model for dual action of V2 in suppressing the host antiviral defense: V2 targets SGS3 for degradation and V2 inhibits CYP1 activity. To study this we proposed to tackle three specific objectives. I. Characterize the role of V2 in SGS3 proteasomal degradation ubiquitination, II. Study the effects of V2 on CYP1 maturation, enzymatic activity, and accumulation and, III. Analyze the effects of the CYP1-V2 interaction on TYLCV-Is infection. Here we describe results from our study that support our hypothesis: the involvement of the host's innate immune system—in this case, PCD—in plant defense against TYLCV-Is. Also, we use TYLCV-Is to discover the molecular pathway(s) by which this plant virus counters this defense. Towards the end of our study we discovered an interesting involvement of the C2 protein encoded by TYLCV-Is in inducing Hypersensitive Response in N. benthamianaplants which is not the case when the whole viral genome is introduced. This might lead to a better understanding of the multiple processes involved in the way TYLCV is overcoming the defense mechanisms of the host plant cell. In a parallel research supporting the main goal described, we also investigated Agrobacteriumtumefaciens-encoded F-box protein VirF. It has been proposed that VirF targets a host protein for the UPS-mediated degradation, very much the way TYLCV V2 does. In our study, we identified one such interactor, an Arabidopsistrihelix-domain transcription factor VFP3, and further show that its very close homolog VFP5 also interacted with VirF. Interestingly, interactions of VirF with either VFP3 or VFP5 did not activate the host UPS, suggesting that VirF might play other UPS-independent roles in bacterial infection. Another target for VirF is VFP4, a transcription factor that both VirF and its plant functional homolog VBF target to degradation by UPS. Using RNA-seqtranscriptome analysis we showed that VFP4 regulates numerous plant genes involved in disease response, including responses to viral and bacterial infections. Detailed analyses of some of these genes indicated their involvement in plant protection against Agrobacterium infection. Thus, Agrobacterium may facilitate its infection by utilizing the host cell UPS to destabilize transcriptional regulators of the host disease response machinery that limits the infection.

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Baszler, Timothy, Igor Savitsky, Christopher Davies, Lauren Staska i Varda Shkap. Identification of bovine Neospora caninum cytotoxic T-lymphocyte epitopes for development of peptide-based vaccine. United States Department of Agriculture, marzec 2006. http://dx.doi.org/10.32747/2006.7695592.bard.

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The goal of the one-year feasibility study was to identify specific cytotoxic T-lymphocyte (CTL) epitopes to Neosporacaninum in the natural bovine host in order to make progress toward developing an effective peptide-based vaccine against bovine neosporosis. We tested the hypothesis that: N. caninum SRS2 peptides contain immunogenicCTLepitope clusters cross-presented by multiple bovine MHC-I and MHC-IIhaplotypes. The specific objectives were: (1) Map bovine CTLepitopes of N. caninum NcSRS-2 and identify consensus MHC-I and class-II binding motifs; and (2) Determine if subunit immunization with peptides containing N. caninum-specificCTLepitopes cross-reactive to multiple bovine MHChaplotypes induces a CTL response in cattle with disparate MHChaplotypes. Neosporosis is a major cause of infectious abortion and congenital disease in cattle, persisting in cattle herds via vertical transmission.5 N. caninum abortions are reported in Israel; a serological survey of 52 Israeli dairy herds with reported abortions indicated a 31% infection rate in cows and 16% infection rate in aborted fetuses.9,14 Broad economic loss due to bovine neosporosis is estimated at $35,000,000 per year in California, USA, and $100,000,000 (Australian) per year in Australia and New Zealand.13 Per herd losses in a Canadian herd of 50 cattle are estimated more conservatively at $2,305 (Canadian) annually.4 Up to date practical measures to reduce losses from neosporosis in cattle have not been achieved. There is no chemotherapy available and, although progress has been made toward understanding immunity to Neospora infections, no efficacious vaccine is available to limit outbreaks or prevent abortions. Vaccine development to prevent N. caninum abortion and congenital infection remains a high research priority. To this end, our research group has over the past decade: 1) Identified the importance of T-lymphocyte-mediated immunity, particularly IFN-γ responses, as necessary for immune protection to congenital neosporosis in mice,1,2,10,11 and 2) Identified MHC class II restricted CD4+ CTL in Neosporainfected Holstein cattle,16 and 3) Identified NcSRS2 as a highly conserved surface protein associated with immunity to Neospora infections in mice and cattle.7,8,15 In this BARD-funded 12 month feasibility study, we continued our study of Neospora immunity in cattle and successfully completed T-lymphocyte epitope mapping of NcSRS2 surface protein with peptides and bovine immune cells,15 fulfilling objective 1. We also documented the importance of immune responses NcSRS2 by showing that immunization with native NcSRS2 reduces congenital Neospora transmission in mice,7 and that antibodies to NcSRS2 specifically inhibition invasion of placental trophoblasts.8 Most importantly we showed that T-lymphocyte responses similar to parasite infection, namely induction of activated IFN-γ secreting Tlymphocytes, could be induced by subunit immunization with NcSRS2 peptides containing the Neospora-specificCTLepitopes (Baszler et al, In preparation) fulfilling objective 2. Both DNA and peptide-based subunit approaches were tested. Only lipopeptide-based NcSRS2 subunits, modified with N-terminal linked palmitic acid to enhance Toll-like receptors 2 and 1 (TLR2-TLR1), stimulated robust antigen-specific T-lymphocyte proliferation, IFN-γ secretion, and serum antibody production across different MHC-IIhaplotypes. The discovery of MHC-II cross-reactive T-cellinducing parasite peptides capable of inducing a potentially protective immune response following subunit immunization in cattle is of significant practical importance to vaccine development to bovine neosporosis. In addition, our findings are more widely applicable in future investigations of protective T-cell, subunit-based immunity against other infectious diseases in outbred cattle populations.

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Zhao, Zepeng, Fengyuan Zhang i Yijin Li. The Relationship Between Il-1 RN intron 2 (VNTR) rs2234663 Gene Polymorphism and The Progression of Periodontitis: A systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, marzec 2023. http://dx.doi.org/10.37766/inplasy2023.3.0100.

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Review question / Objective: The aim of this systematic review and meta-analysis of case-control studies is to find out the association of IL-1 RN intron 2 (VNTR) rs2234663 Gene Polymorphism and the occurrence and progression of periodontitis(including chronic periodontitis, aggressive periodontitis and early-onset periodontitis). Condition being studied: Periodontitis is one of the most common ailments affecting the teeth, leading to the destruction of the supporting and surrounding tooth structure. Periodontitis is originally a disease originating from the gingival tissue which if left untreated results in penetration of inflammation to the deeper tissues, altering the bone homeostasis causing tooth loss. Periodontal disease has a multifactorial origin. The main culprit identified in periodontitis is the bacterial biofilm growing on the tooth surfaces. The deleterious effects of periodontopathogens are not limited to the periodontium, but they also exude their ill effects on the systemic health of the patients. While the host response determines the progression of the disease, genetics, environmental factors, systemic health of the patient, lifestyle habits and various social determinants also play a role. Interleukin-1 receptor antagonist encoded by this gene IL-1RN is a member of the interleukin 1 cytokine family. This protein inhibits the activities of interleukin 1, alpha (IL1A) and interleukin 1, beta (IL1B), and modulates a variety of interleukin 1 related immune and inflammatory responses, particularly in the acute phase of infection and inflammation. We aim to study their association by conducting a meta-analysis.

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