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Journal articles on the topic "Cellular immunity":
1
Jones, Eleanor Livingston, Maria C. Demaria, and Mark D. Wright. "Tetraspanins in cellular immunity." Biochemical Society Transactions 39, no. 2 (March 22, 2011): 506–11. http://dx.doi.org/10.1042/bst0390506.
Tetraspanins are a superfamily of integral membrane proteins involved in the organization of microdomains that consist of both cell membrane proteins and cytoplasmic signalling molecules. These microdomains are important in regulating molecular recognition at the cell surface and subsequent signal transduction processes central to the generation of an efficient immune response. Tetraspanins, both immune-cell-specific, such as CD37, and ubiquitously expressed, such as CD81, have been shown to be imp-ortant in both innate and adaptive cellular immunity. This is via their molecular interaction with important immune cell-surface molecules such as antigen-presenting MHC proteins, T-cell co-receptors CD4 and CD8, as well as cytoplasmic molecules such as Lck and PKC (protein kinase C). Moreover, the generation of tetraspanin-deficient mice has enabled the study of these proteins in immunity. A variety of tetraspanins have a role in the regulation of pattern recognition, antigen presentation and T-cell proliferation. Recent studies have also begun to elucidate roles for tetraspanins in macrophages, NK cells (natural killer cells) and granulocytes.
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Mills, K. H. G., and K. Redhead. "Cellular immunity in pertussis." Journal of Medical Microbiology 39, no. 3 (September 1, 1993): 163–64. http://dx.doi.org/10.1099/00222615-39-3-163.
Fesenko, E. E., V. R. Makar, E. G. Novoselova, and V. B. Sadovnikov. "Microwaves and cellular immunity." Bioelectrochemistry and Bioenergetics 49, no. 1 (October 1999): 29–35. http://dx.doi.org/10.1016/s0302-4598(99)00058-6.
Novoselova, E. G., E. E. Fesenko, V. R. Makar, and V. B. Sadovnikov. "Microwaves and cellular immunity." Bioelectrochemistry and Bioenergetics 49, no. 1 (October 1999): 37–41. http://dx.doi.org/10.1016/s0302-4598(99)00059-8.
Good, Robert A., and Ellen Lorenz. "Nutrition and cellular immunity." International Journal of Immunopharmacology 14, no. 3 (April 1992): 361–66. http://dx.doi.org/10.1016/0192-0561(92)90165-h.
Ячник, І. М., А. В. Бiляєв, and Л. Д. Танцюра. "Multivariable analysis of cellular immunity." Pain, anesthesia and intensive care, no. 4(73) (December 11, 2015): 48–57. http://dx.doi.org/10.25284/2519-2078.4(73).2015.84271.
Network decontamination is a well known mobile agent problem with many applications. We assume that all nodes of a network are contaminated (e.g., by a virus) and a set of agents is deployed to decontaminate them. An agent passing by a node decontaminates it, however a decontaminated node can be recontaminated if any of its neighbours is contaminated. In the vast literature a variety of models are considered and different assumptions are made on the power of the agents.
In this thesis we study variation of the decontamination problem in mesh and tori topologies, under the assumption that when a node is decontaminated, it is immune to recontamination for a predefined amount of time t (called immunity time). After the immunity time is elapsed, recontamination can occur.
We focus on three different models: mobile agents (MA), cellular automata (CA), and mobile cellular automata (MCA). The first two models are commonly studied and employed in several other contexts, the third model is introduced in this thesis for the first time. In each model we study the temporal decontamination problem (adapted to the particular setting) under a variety of assumptions on the capabilities of the decontaminating elements (agents for MA and MCA, decontaminating cells for CA). Some of the parameters we consider in this study are: visibility of the active elements, their ability to make copies of themselves, their ability to communicate, and the possibility to remember their past actions (memory). We describe several solutions in the various scenarios and we analyze their complexity. Efficiency is evaluated slightly differently in each model, but essentially the effort is in the minimization of the number of simultaneous decontaminating elements active in the system while performing the decontamination with a given immunity time.
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Makedonas, George. "Cellular immunity among HIV exposed, uninfected individuals." Thesis, McGill University, 2005. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111828.
Two models of HIV infection have been studied extensively with the goal of identifying immune correlate(s) of protection against HIV: (1) the simian immunodeficiency virus (SIV) infection of rhesus macaque monkeys and (2) individuals with repeated exposure to HIV who remain uninfected by the virus (EUs). Both paradigms suggest that T cell-mediated immunity plays an important role in controlling HIV replication. Evidence from the SIV/macaque system, however, predicts that HIV vaccines aimed at eliciting T cell responses will fail to induce sterilizing immunity against HIV. The aim of the work presented in this thesis was to correlate HIV-specific T cell immunity in EUs with protection from HIV infection. The study cohort was comprised of (a) men who have unprotected sexual intercourse with HIV-infected men (MSM), (b) intravenous drug users (IVDU) who share syringes with HIV-infected peers, and (c) heterosexual partners of HIV-infected subjects. EUs were shown to exhibit HIV-specific IFN-gamma secretion, IL-2 production, and T cell proliferation, whereas low-risk negative controls did not. Furthermore, HIV-specific IFN-gamma secretion and T cell proliferation were not observed among a population of EUs who seroconverted soon after the tested time point. HIV-specific IL-2 secretion and T cell proliferation were shown to be correlated in our cohort of EUs. These effector functions are considered hallmark properties of central memory T cells (TCM), the subset of memory T cells that has been shown to mediate sterilizing immunity in mouse models of viral infection. The presence of TCM in EUs implies the development of immunity against HIV that is either fully protective or partially so, by increasing the threshold for HIV infection. Since these HIV-specific effector functions were absent in EUs who eventually seroconverted, it can be inferred that EUs in our cohort develop HIV-specific T cell immunity that mediates protection from HIV infection. Thus, our contribution to the EU paradigm is that sterilizing immunity is an attainable goal of prospective HIV vaccines.
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Tye, Gee Jun. "Combined adjuvant for stimulation of cellular immunity." Thesis, King's College London (University of London), 2012. https://kclpure.kcl.ac.uk/portal/en/theses/combined-adjuvant-for-stimulation-of-cellular-immunity(b1be07ae-b8d4-40a8-9258-bc3e3413df9d).html.
Vaccination has important clinical potential in the immunotherapy of both infectious disease and cancer. The central aim of the studies reported in this thesis has been the development of vaccination strategies that will be effective for therapeutic applications in cancer. Using ovalbumin antigen in a mouse model, we have examined a combination of recently developed adjuvants referred to as CASAC (combined adjuvants for synergistic stimulation of cellular immunity) to optimise the efficacy of vaccination induced T cell mediated immunity. These studies have examined the effect of repeated rounds of vaccination with one, or alternating cycles of two different helper peptides. The hypothesis was that repeated stimulation of the same clonal population of CD4+ T helper cells with a single MHC class II peptide could induce anergy, exhaustion, clonal deletion and/or stimulation of regulatory T-cells, resulting in reduced and shorter lived immunity. These studies have also examined the effect of inclusion of other immune regulatory components, and in particular a cocktail of cytokines generated by phytohemagglutinin stimulation of human peripheral blood mononuclear cells (referred to as IRX-2). Another important issue for vaccination mediated immune therapy that was addressed is the age-associated loss of immunological competence (immunesenescence). A comparative analysis is reported of the magnitude and duration of responses to vaccination with a single MHC class-I presented peptide in combination with the same or alternating MHC class-II presented peptides. In addition, we have quantified the number of antigen specific CDS T cells, their effector and memory subsets and in vivo antigen specific cytolytic activity to examine the effect of CASAC vaccination alone or in combination with IRX-2. The induction of immunological responses in young and aged immune backgrounds was also examined. Vaccinations with ovalbumin peptides in the CASAC adjuvant have shown higher percentages and numbers of antigen specific CDS T cells with improved cytolytic activity when helper functions are stimulated by two different class-II peptides used in alternating cycles of vaccination, rather than repeated stimulation by the same class-II peptide. This conclusion can be confirmed with a repeated experiment. Analysis of T cells with a regulatory (Treg) phenotype (CD4+CD25+Foxp3+) showed that their expansion was reduced with the alternating T-helper peptide vaccination regimen. The addition of IRX-2 to the CASAC vaccination regimen was found to enhance the in vivo antigen specific cytolytic activity. This was particularly significant in the aged mice which were found to have increased levels of Tregs.
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Patel, Mihil. "Regulation of cellular immunity by human cytomegalovirus." Thesis, Cardiff University, 2018. http://orca.cf.ac.uk/114496/.
The success of HCMV as a lifelong pathogen is attributed at least in part to the broad range of encoded immune evasion molecules that inhibit the host cellular immune response. Indeed, HCMV has become a paradigm for immune evasion, the study of which has revealed a number of basic immunological processes. To screen for novel immune evasion genes, HCMV-specific CD8+ T-cell lines were grown from seropositive donors and used against a series of block deletion viruses, each missing a region of genes non-essential for replication in vitro. UL13-UL20 was flagged as important for inhibition of CD8+ T-cells. Further screening with individual gene knockout HCMVs showed that the published NK-cell inhibitor UL16 could inhibit CD8+ T-cells, but also revealed UL19 as a previously unrecognised strong immune evasin, inhibiting 3 separate CD8+ T-cell lines. UL19 had no effect on HLA-I downregulation indicating that it may affect other pathways involved with T-cell activation. Proteomic data showed that surface TNFR2 was increased by HCMV infection. This is important as this would influence the response to TNF, a major inflammatory cytokine and soluble effector molecule released by T and NK cells. Screening using different HCMV strains and knockout viruses identified UL148 and UL148D as responsible for the increase in surface TNFR2 but prevented the release of soluble TNFR2, indicating that UL148 and UL148D were influencing the ability of TNFR2 to be retained at the cell surface. Infection with HCMV Merlin profoundly downregulated surface ADAM17, the metalloproteinase responsible for cleaving TNFR2 from the cell surface. Deleting UL148 and UL148D recovered ADAM17 expression, blocking the function of which returned surface and soluble TNFR2 levels to those observed with Merlin. This was also true of TNFR1. HCMV infected cell lysates showed that UL148 and UL148D interfered with the maturation of ADAM17. Thus, UL148 and UL148D allow upregulation of TNFR2 and maintain TNFR1 expression during and HCMV infection by impairing surface ADAM17 expression through impairment of ADAM17 maturation. Given that ADAM17 is involved with the cleaving of multiple cytokines, cytokine receptors, adhesion molecules and immune cell receptors, this work identifies a novel mechanism through which HCMV can alter the surface and soluble proteome by preventing the shedding of inflammatory/immune receptors and mediators. More detailed studies will be required to define the global impact of this on the immune system.
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Abuhammash, E. V. "Transfer actor as mediator of cellular immunity." Thesis, Сумський державний університет, 2013. http://essuir.sumdu.edu.ua/handle/123456789/32144.
Transfer factor (s) - are small molecules, that transfer the ability to recognize pathogens (bacterial or viral) cells of the immune system, never exposed to this pathogen.
When you are citing the document, use the following link http://essuir.sumdu.edu.ua/handle/123456789/32144
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Oldenhove, Guillaume. "Contrôle de la réponse immunitaire induite par les cellules dendritiques: rôle des cellules T régulatrices naturelles ou induites." Doctoral thesis, Universite Libre de Bruxelles, 2006. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/210888.
Weber, Wilhelm Evert Jacob. "Cellular auto-immunity in central nervous system disease." Maastricht : Maastricht : Rijksuniversiteit Limburg ; University Library, Maastricht University [Host], 1988. http://arno.unimaas.nl/show.cgi?fid=5594.
Nickless, Jane Christina. "Cellular immunity to acetylcholine receptor in myasthenia gravis." Thesis, University of Bath, 1985. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.767550.
Nicotinic acetylcholine receptor (AChR) has been purified from Torpedo electric organ, foetal calf muscle, adult human leg muscle, and foetal human skeletal muscle, by extraction in non-ionic detergent followed by affinity purification on immobilised a-toxin. The purified AChR preparations were used to study cellular responses in vitro from patients with myasthenia gravis. In addition, several characterisation studies were carried out on the foetal calf AChR preparation. Purified foetal calf AChR was shown in isoelectric focussing experiments to focus as a single sharp peak at pH 5.2 +/- 0.1, and the receptor sedimented in sucrose density gradients as a single species with a sedimentation coefficient S20w= 9.35 +/- 0.10 S, when indirectly labelled with [125 I]-a-bungarotoxin. SDS-polyacrylamide gel electrophoresis of purified foetal calf AChR consistently showed five major protein bands with (Mr) 40, 44, 47, 52 and 57 K. The 57K protein sub-unit was always the most prominent band. A procedure by which to measure antigen-specific lymphocyte proliferation in vitro was developed and optimised in a system using tetanus toxoid and peripheral blood mononuclear leucocytes (PBL) from a normal donor recently immunised against tetanus. Conditions for the production of human T-cell growth factor (TCGF), or Interleukin 2 (IL-2) were optimised, and used in the tetanus toxoid system to develop a procedure by which antigen-specific reactive T-lymphocytes could be isolated, expanded into long-term lines, and ultimately cloned. Antigen and TCGF were required for the expansion and maintenance of the T-cell lines and clones. The AChR purification procedure was modified several times in order to obtain a workable, non-inhibitory AChR preparation for studies of myasthenia gravis in vitro. Lymphocytes, collected from myasthenic blood samples, were shown to proliferate weakly in response to purified AChR added in vitro, with a mean stimulation index (+/- SEM) of 1.72 +/- 0.12. The proliferative response did not appear to be related to the species of AChR employed, age, sex, or clinical classification of the patient, but higher stimulation indices were obtained from patients in a state of disease exacerbation at the time the sample was taken. T-cell fractionation, or reactive T-cell pre-selection steps, did not enhance the proliferative response of myasthenic lymphocytes to purified AChR in vitro, and attempts to isolate and expand AChR-autoreactive T-lymphocytes using antigen and IL-2 were unsuccessful.
Federation of Immunological Societies of Asia-Oceania. Congress. 2nd Congress of the Federation of Immunological Societies of Asia-Oceania: Bangkok, Thailand, January 23-27, 2000. Edited by Sirisinha Stitaya, Chaiyaroj Sansanee C, and Tapchaisri Pramuan. Bologna, Italy: Monduzzi Editore, International Proceedings Division, 2000.
International Lymphokine Workshop ((4th 1984 Schloss Elmau). Cellular and molecular biology of lymphokines: Proceedings of the Fourth International Lymphokine Workshop. Edited by Sorg Clemens, Schimpl Anneliese, and Landy Maurice. Orlando: Academic Press, 1985.
Felippe, Julia B. "Cellular Immunity." In Interpretation of Equine Laboratory Diagnostics, 267–72. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2017. http://dx.doi.org/10.1002/9781118922798.ch45.
Tzianabos, Arthur O., and Lee M. Wetzler. "Cellular Communication." In Immunology, Infection, and Immunity, 343–69. Washington, DC, USA: ASM Press, 2015. http://dx.doi.org/10.1128/9781555816148.ch15.
Nauta, Jozef. "Humoral and Cellular Immunity." In Springer Series in Pharmaceutical Statistics, 15–19. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-37693-2_2.
Nauta, Jozef. "Humoral and Cellular Immunity." In Statistics in Clinical Vaccine Trials, 13–17. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-14691-6_2.
Goodwin, James S., and Jan L. Ceuppens. "Prostaglandins, Cellular Immunity and Cancer." In Prostaglandins and Immunity, 1–34. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2603-8_1.
Troilo, Arianna, Nadezhda Camacho-Ordonez, Chiara Della Bella, and Mario Milco D’Elios. "Mucosal Immunity in Primary Immunodeficiencies." In Cellular Primary Immunodeficiencies, 65–74. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-70107-9_5.
Söderhäll, Kenneth, and Anna Aspán. "Prophenoloxidase Activating System and Its Role in Cellular Communication." In Insect Immunity, 113–29. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-1618-3_9.
Alsina, Laia, Carlos Rodriguez-Gallego, Ana Esteve-Solé, Alexandru Vlagea, Rebeca Pérez de Diego, Rubén Martínez-Barricarte, and Àngela Deyà-Martínez. "Defects in Intrinsic and Innate Immunity." In Cellular Primary Immunodeficiencies, 177–212. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-70107-9_8.
Solomon, S. R., and A. J. Barrett. "Reconstituting T Cell Immunity Following Hematopoietic Stem Cell Transplantation." In Cellular Engineering and Cellular Therapies, 161–69. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4757-3718-9_14.
Yadav, Meena. "Innate Immunity." In An Interplay of Cellular and Molecular Components of Immunology, 27–59. Boca Raton: CRC Press, 2022. http://dx.doi.org/10.1201/9781003286424-2.
Conference papers on the topic "Cellular immunity":
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Hentley, William Thomas. "Bedbug cellular immunity." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.109396.
Pittet, Mikael. "Abstract IA04: Cancer-promoting immunity." In Abstracts: AACR Special Conference on Cellular Heterogeneity in the Tumor Microenvironment; February 26 — March 1, 2014; San Diego, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.chtme14-ia04.
Zhuravlev, Viacheslav, Marina Dyakova, Dilyara Esmedlyaeva, and Tatiana Perova. "Markers of cellular immunity in the diagnosis of tuberculosis pleurisy." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa2711.
Tyumonbaeva, N. B., A. A. Kazybekova, N. J. Mamytova, and A. J. Myrzakulova. "Peculiarities of immunophysiological shifts in adaptation to climatic and geographical conditions of mountains." In VIII Vserossijskaja konferencija s mezhdunarodnym uchastiem «Mediko-fiziologicheskie problemy jekologii cheloveka». Publishing center of Ulyanovsk State University, 2021. http://dx.doi.org/10.34014/mpphe.2021-198-201.
The functioning of the immune system of people exposed to prolonged exposure to natural factors has been monitored and the main immunity indicators have been studied in practically healthy population of different mountain heights in Chui and Naryn regions. Indicators of specific immunity in the residents of the zone of compensated discomfort is reduced compared with the standards of the zone of relative comfort and refers to the mixed type with suppression of cellular and humoral immunity, apparently, this is associated with the climatic and geographical and environmental characteristics of the region.
Key words: adaptation, immune system, T- lymphocytes, B- lymphocytes, immunoglobulins, circulating immune complexes, mountainous conditions.
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Jiang, Haiying, Yougang Gao, and Dan Zhang. "Study on Digital Cellular Mobile Communication System Receiver's Immunity to Interference." In 2010 6th International Conference on Wireless Communications, Networking and Mobile Computing (WiCOM). IEEE, 2010. http://dx.doi.org/10.1109/wicom.2010.5600603.
Antanovich, Zhanna, and Natalia Goncharova. "The features of cellular immunity in patients with treatment-resistant asthma." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa570.
Huang, Jia. "Roles of biogenic amine receptors in insect hemocytes to regulate cellular immunity." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.93036.
Zhiba, G. V., V. P. Pisarenko, and A. N. Shevtsov. "Improve Noise Immunity of Transfer Messages by Radio Channel in Cellular Systems." In 2018 International Multi-Conference on Industrial Engineering and Modern Technologies (FarEastCon). IEEE, 2018. http://dx.doi.org/10.1109/fareastcon.2018.8602932.
Park, Youngjin. "Eicosanoid signaling involved in expression of NADPH-dependent oxidase in insect cellular immunity." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.94764.
Razumnyi, Roman, and Kateryna Gashynova. "Condition of cellular immunity in patients with prolonged course of community acquired pneumonia." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.2328.
Lillehoj, Hyun, Dan Heller, and Mark Jenkins. Cellular and molecular identification of Eimeria Acervulina Merozoite Antigens eliciting protective immunity. United States Department of Agriculture, November 1992. http://dx.doi.org/10.32747/1992.7561056.bard.
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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Hrushesky, William J. Preliminary Investigation of the Role of Cellular Immunity in Estrous Cycle Modulation of Post-Resection Breast Cancer Spread. Fort Belvoir, VA: Defense Technical Information Center, December 2002. http://dx.doi.org/10.21236/ada415581.
Hrushesky, William J. Preliminary Investigation of the Role of Cellular Immunity in Estrous Cycle Modulation of Post-Resection Breast Cancer Spread. Fort Belvoir, VA: Defense Technical Information Center, May 2003. http://dx.doi.org/10.21236/ada421466.
Hrushesky, William J. Preliminary Investigation of the Role of Cellular Immunity in Estrous Cycle Modulation of Post-Resection Breast Cancer Spread. Fort Belvoir, VA: Defense Technical Information Center, May 1999. http://dx.doi.org/10.21236/ada392521.
Bercovier, Herve, Raul Barletta, and Shlomo Sela. Characterization and Immunogenicity of Mycobacterium paratuberculosis Secreted and Cellular Proteins. United States Department of Agriculture, January 1996. http://dx.doi.org/10.32747/1996.7573078.bard.
Our long-term goal is to develop an efficient acellular vaccine against paratuberculosis based on protein antigen(s). A prerequisite to achieve this goal is to analyze and characterize Mycobacterium paratuberculosis (Mpt) secreted and cellular proteins eliciting a protective immune response. In the context of this general objective, we proposed to identify, clone, produce, and characterize: the Mpt 85B antigen and other Mpt immunoreactive secreted proteins, the Mpt L7/L12 ribosomal protein and other immunoreactive cellular proteins, Mpt protein determinants involved in invasion of epithelial cells, and Mpt protein antigens specifically expressed in macrophages. Paratuberculosis is still a very serious problem in Israel and in the USA. In the USA, a recent survey evaluated that 21.6% of the dairy herd were infected with Mpt resulting in 200-250 million dollars in annual losses. Very little is known on the virulence factors and on protective antigens of Mpt. At present, the only means of controlling this disease are culling or vaccination. The current vaccines do not allow a clear differentiation between infected and vaccinated animals. Our long-term goal is to develop an efficient acellular paratuberculosis vaccine based on Mpt protein antigen(s) compatible with diagnostic tests. To achieve this goal it is necessary to analyze and characterize secreted and cellular proteins candidate for such a vaccine. Representative Mpt libraries (shuttle plasmid and phage) were constructed and used to study Mpt genes and gene products described below and will be made available to other research groups. In addition, two approaches were performed which did not yield the expected results. Mav or Mpt DNA genes that confer upon Msg or E. coli the ability to invade and/or survive within HEp-2 cells were not identified. Likewise, we were unable to characterize the 34-39 kDa induced secreted proteins induced by stress factors due to technical difficulties inherent to the complexity of the media needed to support substantial M. pt growth. We identified, isolated, sequenced five Mpt proteins and expressed four of them as recombinant proteins that allowed the study of their immunological properties in sensitized mice. The AphC protein, found to be up regulated by low iron environment, and the SOD protein are both involved in protecting mycobacteria against damage and killing by reactive oxygen (Sod) and nitrogen (AhpC) intermediates, the main bactericidal mechanisms of phagocytic cells. SOD and L7/L12 ribosomal proteins are structural proteins constitutively expressed. 85B and CFP20 are both secreted proteins. SOD, L7/L12, 85B and CFP20 were shown to induce a Th1 response in immunized mice whereas AphC was shown by others to have a similar activity. These proteins did not interfere with the DTH reaction of naturally infected cows. Cellular immunity provides protection in mycobacterial infections, therefore molecules inducing cellular immunity and preferentially a Th1 pathway will be the best candidate for the development of an acellular vaccine. The proteins characterized in this grant that induce a cell-mediated immunity and seem compatible with diagnostic tests, are good candidates for the construction of a future acellular vaccine.
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Chejanovsky, Nor, and Bruce A. Webb. Potentiation of pest control by insect immunosuppression. United States Department of Agriculture, July 2004. http://dx.doi.org/10.32747/2004.7587236.bard.
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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Evans, Donald L., Avigdor Eldar, Liliana Jaso-Friedmann, and 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, February 2005. http://dx.doi.org/10.32747/2005.7586538.bard.
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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Chejanovsky, Nor, and Bruce A. Webb. Potentiation of Pest Control by Insect Immunosuppression. United States Department of Agriculture, January 2010. http://dx.doi.org/10.32747/2010.7592113.bard.
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.
