Relevant bibliographies by topics / Immunogeni

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Immunogeni'

Author: Grafiati
Published: 11 March 2023

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Journal articles on the topic "Immunogeni"

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Gneiss, C., P. Tripp, F. Reichartseder, R. Egg, R. Ehling, A. Lutterotti, M. Khalil, et al. "Differing immunogenic potentials of interferon beta preparations in multiple sclerosis patients." Multiple Sclerosis Journal 12, no. 6 (November 2006): 731–37. http://dx.doi.org/10.1177/1352458506070941.

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Interferon beta (IFNβ) is a first-line therapy for multiple sclerosis (MS). However, some patients experience a decline in efficacy with continued therapy due to the development of anti-IFNβ neutralizing antibodies (NAb). We investigated the frequency of NAb cross-sectionally in 846 MS patients who were receiving IFNβ-1b, IFNβ-1a im, or IFNβ-1a sc. The frequency of NAb in patients receiving IFNβ-1a im was lower (5%) than in patients treated with any other form of IFNβ (22-35%) (P < 0.0001). Binding antibodies (BAb) were measured in 808 patients. The frequency differed significantly between treatment groups, ranging from 45% (IFNβ-1a im) to 88% (IFNβ-1b). The proportion of NAb-positive patients within the BAb-positive group differed significantly among treatment groups, ranging between 12% (IFNβ-1a im) and 51% (IFNβ-1a sc). The median NAb titer from all IFNβ-1a-treated patients was higher than from IFNβ-1b-treated patients (446 versus 171 NU/mL, P = 0.04). Among NAb-positive patients, the frequency of NAb titers > 100 NU/mL was 71% for IFNβ-1a compared with 58% for IFNβ-1b (P = 0.04). Except for conflicting data regarding IFNβ-1a sc, the results are generally consistent with the literature and together with the differing proportion of NAb-positive patients within the BAb-positive group, provide further insight into the immunogeni-city of the IFNβ preparations.
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Tuveson, D. A., J. M. Ahearn, A. K. Matsumoto, and D. T. Fearon. "Molecular interactions of complement receptors on B lymphocytes: a CR1/CR2 complex distinct from the CR2/CD19 complex." Journal of Experimental Medicine 173, no. 5 (May 1, 1991): 1083–89. http://dx.doi.org/10.1084/jem.173.5.1083.

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The complement system augments the humoral immune response to low concentrations of antigen. This effect may be partly mediated by complement receptors on the surface of B lymphocytes that bind immunogenic complexes bearing fragments of C3 and C4. We have shown by immunoprecipitation analysis that the two complement receptors expressed by B lymphocytes, complement receptor 1 (CR1) and CR2, form a detergent-sensitive complex on the surface of tonsillar B lymphocytes and on K562 erythroleukemia cells that were co-transfected with cDNAs encoding CR1 and CR2. The CR1/CR2 complex is distinct from the CR2/CD19 complex and may assist B cell activation by efficiently capturing C3b-containing immunogens and maintaining such immunogens on the B cell after CR1 and factor I-mediated cleavage to iC3b and C3dg. The complement activating immunogen may then trigger signal transduction by the CR1/CR2 complex, the CR2/CD19 complex, or membrane immunoglobulin.
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&NA;. "Synthetic HIV peptide immunogen ???safe??? and immunogenic." Inpharma Weekly &NA;, no. 1152 (August 1998): 8. http://dx.doi.org/10.2165/00128413-199811520-00014.

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Weaver, Eric A., Zhongjing Lu, Zenaido T. Camacho, Fatiha Moukdar, Hua-Xin Liao, Ben-Jiang Ma, Mark Muldoon, et al. "Cross-Subtype T-Cell Immune Responses Induced by a Human Immunodeficiency Virus Type 1 Group M Consensus Env Immunogen." Journal of Virology 80, no. 14 (July 15, 2006): 6745–56. http://dx.doi.org/10.1128/jvi.02484-05.

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ABSTRACT The genetic diversity among globally circulating human immunodeficiency virus type 1 (HIV-1) strains is a serious challenge for HIV-1 vaccine design. We have generated a synthetic group M consensus env gene (CON6) for induction of cross-subtype immune responses and report here a comparative study of T-cell responses to this and natural strain env immunogens in a murine model. Three different strains of mice were immunized with CON6 as well as subtype A, B, or C env immunogens, using a DNA prime-recombinant vaccinia virus boost strategy. T-cell epitopes were mapped by gamma interferon enzyme-linked immunospot analysis using five overlapping Env peptide sets from heterologous subtype A, B, and C viruses. The CON6-derived vaccine was immunogenic and induced a greater number of T-cell epitope responses than any single wild-type subtype A, B, and C env immunogen and similar T-cell responses to a polyvalent vaccine. The responses were comparable to within-clade responses but significantly more than between-clade responses. The magnitude of the T-cell responses induced by CON6 (measured by individual epitope peptides) was also greater than the magnitude of responses induced by individual wild-type env immunogens. Though the limited major histocompatibility complex repertoire in inbred mice does not necessarily predict responses in nonhuman primates and humans, these results suggest that synthetic centralized env immunogens represent a promising approach for HIV-1 vaccine design that merits further characterization.
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Campbell, M. J., W. Carroll, S. Kon, K. Thielemans, J. B. Rothbard, S. Levy, and R. Levy. "Idiotype vaccination against murine B cell lymphoma. Humoral and cellular responses elicited by tumor-derived immunoglobulin M and its molecular subunits." Journal of Immunology 139, no. 8 (October 15, 1987): 2825–33. http://dx.doi.org/10.4049/jimmunol.139.8.2825.

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Abstract C3H/HeN mice were immunized with idiotypic immunoglobulin M (IgM) and its molecular subunits from the syngeneic 38C13 lymphoma. Immunization with idiotypic IgM (38C-Id) resulted in idiotype-specific humoral and cellular immunity and protection against a lethal tumor cell challenge. Heavy (H38C) and light (L38C) chains were isolated by electroelution from preparative polyacrylamide gels. Both of these immunogens induced significant resistance to a subsequent tumor challenge. Variable region immunogens, in the form of trpE-fusion proteins, were obtained by cloning heavy and light chain variable region genes into the expression plasmid pATH-11. Of these, only the trpE-VH38C immunogen yielded immune resistance to tumor challenge. Finally, the nucleic acid sequence of 38C-Id light chain was determined and, based on the corresponding amino acid sequence and an analysis of predicted secondary structure, a region of potential antigenicity in complementarity-determining region 3 was chosen for the production of a synthetic peptide. Vaccination with this synthetic peptide resulted in significant suppression of tumor growth. Analysis of the humoral and cellular immunity generated by these vaccines revealed the presence of antibodies reactive with native idiotypic IgM only in 38C-Id, H38C, and trpE-VH38C immune sera, although the latter two were not idiotype-specific. Idiotype-specific lymphocytes, which proliferated in response to native 38C-Id, were observed in all immune animals. With the exception of the fusion protein immunogens, conjugation to an immunogenic carrier protein (keyhole limpet hemocyanin or thyroglobulin) was required for optimal humoral and cellular responses.
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Noh, Susan M., Joshua E. Turse, Wendy C. Brown, Junzo Norimine, and Guy H. Palmer. "Linkage between Anaplasma marginale Outer Membrane Proteins Enhances Immunogenicity but Is Not Required for Protection from Challenge." Clinical and Vaccine Immunology 20, no. 5 (February 27, 2013): 651–56. http://dx.doi.org/10.1128/cvi.00600-12.

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ABSTRACTThe prevention of bacterial infections via immunization presents particular challenges. While outer membrane extracts are often protective, they are difficult and expensive to isolate and standardize and thus are often impractical for development and implementation in vaccination programs. In contrast, individual proteins, which are easily adapted for use in subunit vaccines, tend to be poorly protective. Consequently, identification of the specific characteristics of outer membrane-based immunogens, in terms of the antigen contents and contexts that are required for protective immunity, represents a major gap in the knowledge needed for bacterial vaccine development. Using as a modelAnaplasma marginale, a persistent tick-borne bacterial pathogen of cattle, we tested two sets of immunogens to determine whether membrane context affected immunogenicity and the capacity to induce protection. The first immunogen was composed of a complex of outer membrane proteins linked by covalent bonds and known to be protective. The second immunogen was derived directly from the first one, but the proteins were individualized rather than linked. The antibody response induced by the linked immunogen was much greater than that induced by the unlinked immunogen. However, both immunogens induced protective immunity and an anamnestic response. These findings suggest that individual proteins or combinations of proteins can be successfully tested for the ability to induce protective immunity with less regard for overall membrane context. Once protective antigens are identified, immunogenicity could be enhanced by cross-linking to allow a reduced immunogen dose or fewer booster vaccinations.
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Das, Supratik, Rajesh Kumar, Shubbir Ahmed, Hilal Ahmad Parray, and Sweety Samal. "Efficiently cleaved HIV-1 envelopes: can they be important for vaccine immunogen development?" Therapeutic Advances in Vaccines and Immunotherapy 8 (January 2020): 251513552095776. http://dx.doi.org/10.1177/2515135520957763.

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The enormous diversity of HIV-1 is a significant impediment in selecting envelopes (Envs) that can be suitable for designing vaccine immunogens. While tremendous progress has been made in developing soluble, trimeric, native-like Env proteins, those that have elicited neutralizing antibodies (Abs) in animal models are relatively few. A strategy of selecting naturally occurring Envs suitable for immunogen design by studying the correlation between efficient cleavage on the cell surface and their selective binding to broadly neutralizing Abs (bNAbs) and not to non-neutralizing Abs (non-NAbs), properties essential in immunogens, may be useful. Here we discuss some of the challenges of developing an efficacious HIV-1 vaccine and the work done in generating soluble immunogens. We also discuss the study of naturally occurring, membrane-bound, efficiently cleaved (naturally more sensitive to furin) Envs and how they may positively add to the repertoire of HIV-1 Envs that can be used for vaccine immunogen design. However, even with such Envs, the challenges of developing well-folded, native-like trimers as soluble proteins or using other immunogen strategies such as virus-like particles with desirable antigenic properties remain, and are formidable. In spite of the progress that has been made in the HIV-1 vaccine field, an immunogen that elicits neutralizing Abs with significant breadth and potency in vaccines has still not been developed. Efficiently cleaved Envs may increase the number of available Envs suitable for immunogen design and should be studied further.
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Watson, Douglas, and Francis Szoka. "Role of lipid structure in the humoral immune response in mice to covalent lipid-peptides derived from the membrane proximal region of HIV-1 gp41 (128.2)." Journal of Immunology 182, no. 1_Supplement (April 1, 2009): 128.2. http://dx.doi.org/10.4049/jimmunol.182.supp.128.2.

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Abstract The membrane proximal region (MPR) of HIV-1 gp41 is a desirable target for development of a vaccine that elicits neutralizing antibodies since the patient-derived monoclonal antibodies, 2F5 and 4E10, bind to MPR and neutralize primary isolates. The 2F5 and 4E10 antibodies cross-react with lipids and structural studies suggest that MPR immunogens may be presented in a membrane environment. We hypothesized that covalent attachment of lipid anchors would enhance the immunogenicity of MPR-derived peptides presented in liposomal bilayers. In a comparison of eight different lipids conjugated to an extended 2F5 epitope peptide, a sterol, cholesterol hemisuccinate (CHEMS), was found to promote the strongest anti-peptide immune response in BALB/C mice. Differences in immunogenicity amongst the conjugates could not be explained solely by any one factor, such as: the presence of a phosphate in the lipid, membrane partitioning of the lipid anchor or peptide secondary structure. Conjugation to CHEMS also rendered a 4E10 epitope peptide immunogenic. Finally, conjugation of CHEMS to a helically constrained immunogen spanning both epitopes elicited antibodies that bound to each of the individual 4E10 and 2F5 epitopes as well as to an oligomeric recombinant envelope protein. Further research into the mechanism of how structure influences the immune response to the MPR may lead to immunogens that could be useful in prime-boost regimens for focusing the immune response in an HIV vaccine.
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Letvin, Norman L., Yue Huang, Bimal K. Chakrabarti, Ling Xu, Michael S. Seaman, Kristin Beaudry, Birgit Korioth-Schmitz, et al. "Heterologous Envelope Immunogens Contribute to AIDS Vaccine Protection in Rhesus Monkeys." Journal of Virology 78, no. 14 (July 15, 2004): 7490–97. http://dx.doi.org/10.1128/jvi.78.14.7490-7497.2004.

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ABSTRACT Because a strategy to elicit broadly neutralizing anti-human immunodeficiency virus type 1 (HIV-1) antibodies has not yet been found, the role of an Env immunogen in HIV-1 vaccine candidates remains undefined. We sought to determine whether an HIV-1 Env immunogen genetically disparate from the Env of the challenge virus can contribute to protective immunity. We vaccinated Indian-origin rhesus monkeys with Gag-Pol-Nef immunogens, alone or in combination with Env immunogens that were either matched or mismatched with the challenge virus. These animals were then challenged with a pathogenic simian-human immunodeficiency virus. The vaccine regimen included a plasmid DNA prime and replication-defective adenoviral vector boost. Vaccine regimens that included the matched or mismatched Env immunogens conferred better protection against CD4+ T-lymphocyte loss than that seen with comparable regimens that did not include Env immunogens. This increment in protective immunity was associated with anamnestic Env-specific cellular immunity that developed in the early days following viral challenge. These data suggest that T-lymphocyte immunity to Env can broaden the protective cellular immune response to HIV despite significant sequence diversity of the strains of the Env immunogens and can contribute to immune protection in this AIDS vaccine model.
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Yu, Zhe, Li Liu, Xiaobo Yu, Jun Chi, Huanhuan Han, Ying Liu, Wei He, Qihong Sun, Jianen Gao, and Danke Xu. "High-Throughput Antibody Generation Using Multiplexed Immunization and Immunogen Array Analysis." Journal of Biomolecular Screening 15, no. 10 (December 2010): 1260–67. http://dx.doi.org/10.1177/1087057110380045.

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In this work, the authors developed a new screening approach using multiplexed immunization and immunogen array analysis to improve the efficiency of antibody screening for high-throughput antibody generation. The immunogen array is based on a 96-well format in which different immunogens and negative as well as positive controls are immobilized in each well, thus making it possible to screen hundreds of antibody candidates simultaneously. To demonstrate this approach, a model of 4 mixed immunogens immunization was employed. In total, 675 antibody candidates were screened before and after established antibody hybridomas in parallel with immunogen arrays and enzyme-linked immunosorbent assay. The signal intensity, specificity, and cross-reactivity of produced antibody candidates were analyzed using a hierarchical cluster algorithm to track the characteristics of antibody candidates during antibody generation, which might reduce the number of false-positive and false-negative binding of antibodies. Moreover, 4 monoclonal antibodies that were produced successfully recognized their corresponding target antigens.
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Dissertations / Theses on the topic "Immunogeni"

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Sukkurwala, Abdul Qader. "Autophagy : A New Modulator of Immunogenic Cell Death for Cancer Therapy." Thesis, Paris 11, 2013. http://www.theses.fr/2013PA11T031.

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Certains agents chimiothérapeutiques tels que les anthracyclines ou l'oxaliplatine induisent une mort cellulaire immunogène, ce qui implique que les cellules mourrantes du patient servent de vaccin thérapeutique en stimulant une réponse immunitaire antitumorale. La mort cellulaire immunogène est caractérisée par la libération de signaux d'alarme par la cellule tumorale mourante qui permettent l’activation du système immunitaire. En premier lieu, l'exposition de la calréticuline à la surface de la cellule tumorale mourante va agir comme un signal de type «eat-me» pour les cellules dendritiques. Une fois relâchée, la protéine nucléaire HMGB1 se lie au récepteur TLR4 afin de faciliter la présentation antigénique. Les cellules mourantes vont également libérer de l'ATP qui agit sur les récepteurs P2X7 et active l’inflammasomme NLRP3, conduisant à la libération d'IL-1β et ainsi à l’activation des cellules T CD8+ productrices d’IFN-γ. L’autophagie est un mécanisme cellulaire qui est activé en réponse à la chimiothérapie. L'autophagie signifie «self-ating», il s'agit d'un processus cellulaire activé par diverses conditions de stress, par lequel les cellules peuvent dégrader les protéines et les organites. Il peut aussi être induit par un stress du réticulum endoplasmique. Ce dernier étant également impliqué dans l'exposition de la calréticuline pendant la mort cellulaire immunogène, nous avons au cours de cette étude cherché à déterminer le rôle de l'autophagie dans la mort cellulaire immunogène. Nous avons constaté que l'autophagie est nécessaire pour la libération de l'ATP après un traitement par des chimiothérapies immunogènes, en observant que le nockdown de gènes essentiels de l'autophagie limitait la sécrétion d'ATP. Nous avons également observé que des cellules déficientes pour l'autophagie traitées par une chimiothérapie immunogène sont incapables d’immuniser des souris contre une injection de cellules vivantes. En outre, les tumeurs déficientes pour l’autophagie ne répondent pas à un traitement systémique immunogène dans des souris immunocompétentes et continuent à proliférer en comparaison à des tumeurs “wild-type”. De plus, nous avons montré que les cellules déficientes pour l'autophagie ne sont pas en mesure de recruter des cellules dendritiques dans le lit tumoral ou d'induire l’activation des cellules T CD8+. A l'inverse, l'inhibition des enzymes de dégradation de l’ATP extracellulaire accroit les concentrations d'ATP dans les tumeurs déficientes pour l'autophagie, ce qui rétablit le recrutement des cellules immunitaires dans le lit tumoral et restaure la réponse chimiothérapeutique des cancers déficients pour l'autophagie. Ainsi, cette étude a montré l'importance de l'autophagie dans la réponse anti-tumorale spécifique, après traitement par des chimiothérapies immunogènes. Ces résultats ouvrent de nouvelles perspectives dans le concept de la mort cellulaire immunogène
In recent years it has been demonstrated that some chemotherapeutic agents such as anthracyclines or oxaliplatin can induce a type of tumor cell death that is immunogenic, implying that the patient’s dying cancer cells serve as a therapeuticvaccine that stimulates an antitumor immune response, which in turn can control or eradicate residual cancer cells. Immunogenic cell death is characterized by the emission of danger signals from the dying tumor cell, which activate the immune system. At first the exposure of calreticulin, acts as an «eat-me» signal for dendritic cells (DCs). Once released, the nuclear protein HMGB1 binds to TLR4 on DCs, facilitating antigen processing and presentation. The dying tumor cells also releases ATP, which acts on P2X7 receptors on DCs and activates the NLRP3 inflammasome, leading to IL-1β release, necessary for IFN-γ-producing CD8+ T cell activation. Autophagy literally ‘self-eating’ is a cellular process activated in response to various conditions of cellular stress, whereby cells can liberate energy resources via the degradation of proteins and organelles. Recently autophagy has been found activated in response to chemotherapy and in this project we aimed to determine the potential role of autophagy in immunogenic cell death. We found that autophagy isrequired for the release of ATP in response to immunochemotherapeutic treatment, as we observed that the knockdown of essential autophagy-related genes abolished its secretion. We observed that autophagy deficient cells treated with immunogenic cell death inducers failed to immunize mice against a re-challenge with living cells. Furthermore, autophagy deficient tumors growing on immunocompetent mice did not respond to systemic immunogenic treatment and continued proliferating in contrast to autophagy proficient tumors. We showed that autophagy deficient cells were neither able to recruit DCs into the tumor bed nor to activate CD8+ T cells. Conversely, the inhibition of extracellular ATP degrading enzymes increased extracellular ATP concentrations in autophagy deficient tumors, which reestablished the recruitment of immune cells into the tumor bed, and restored chemotherapeutic responses in autophagy-deficient cancers. Altogether, this study showed the importance of autophagy in tumor-specific immune response after treatment with chemotherapy, thus giving new insights into the concept of immunogenic cell death
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Menger, Laurie Colombe Aude. "Effets anticancereux des glucosides cardiotoniques par induction d'une mort cellulaire immunogène." Phd thesis, Université Paris Sud - Paris XI, 2012. http://tel.archives-ouvertes.fr/tel-00757180.

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L'efficacité de certains agents anti-cancéreux, notamment les anthracyclines et l'oxaliplatine repose sur l'induction d'une mort cellulaire immunogène (MCI) pouvant conduire à une réponse immunitaire anti-tumorale spécifique. Les cellules succombant à ce type particulier d'apoptose vont subir certaines modifications définies par un modèle spatio-temporel précis. Celui-ci est caractérisé par la mise en place de signaux d'apparition séquentielle, dont le plus précoce est l'exposition membranaire d'une protéine du réticulum endoplasmique, la calréticuline (CRT) qui constitue un signal de danger essentiel à la phagocytose des cellules mourantes par les cellules dendritiques. Ensuite, à un stade apoptotique, la sécrétion d'adénosine triphosphate (ATP) dépendante de l'autophagie active l'inflammasome NLRP3 et induit la polarisation des cellules T CD8+ productrices d'IFN-. Enfin, au cours de la nécrose secondaire, le relargage d'un facteur pro-immunogène High-mobility group protein B1 (HMGB1) est indispensable à une présentation antigénique optimale aux cellules T CD4+ et CD8+, contribuant ainsi à l'activité tumoricide de la chimiothérapie et protégeant l'hôte d'une éventuelle rechute. De manière à identifier de nouvelles molécules capables d'induire une réponse immunitaire anti-tumorale spécifique, un criblage à haut débit de bibliothèques de composés approuvés par la FDA (Food and Drug Administration) a été réalisé grâce à l'utilisation de microscopie automatisée et de biosenseurs permettant la détection de l'exposition de la CRT, de la sécrétion d'ATP et du relargage d'HMGB1. Ce criblage multiparamétrique à haut débit a permis d'identifier les glucosides cardiotoniques (GCs), déjà bien connus pour leur activité cytotoxique préférentielle des cellules cancéreuses, comme étant des inducteurs efficaces de la MCI. Cette découverte a été validée par des méthodes alternatives in vitro, suivis d'une étude de la mécanistique d'induction de la MCI par les GCs. Les résultats ont mis en évidence une inhibition spécifique de la sous-unité α1 de la pompe Na + / K + ATPase, qui à son tour modifie l'homéostasie calcique de la cellule cible, un effet reproduit par les ionophores du Ca2 +. Nous avons ensuite montré que les CGs, en combinaison avec des chimiothérapies non immunogènes (cisplatine ou mitomycine C) pouvaient vacciner des souris syngéniques contre une ré-injection de cellules cancéreuses vivantes et que les effets antinéoplastiques de ces agents endommageants l'ADN pouvaient être potentialisés par les GCs dans les hôtes immunocompétents mais pas dans les souris immunodéficientes. Enfin, une analyse rétrospective de patients atteints de carcinomes et traités par un GC couramment utilisé en clinique dans la prise en charge de l'insuffisance cardiaque, la digoxine (n=145) a révélé une amélioration significative de la survie globale par rapport à celle de patients non traités (n=290). Les patients ont été appariés en fonction de leur âge, sexe, type de cancer et principaux paramètres pronostiques. Des analyses plus approfondies ont ensuite révélées que la digoxine n'affectait pas la survie globale des patients déjà traités par des agents chimiothérapeutiques immunogènes mais celle des patients ayant reçu des agents autres que les anthracyclines ou l'oxaliplatine.
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Zhou, Heng. "Mode d'action des composés induits Lytix sur la mort cellulaire." Thesis, Université Paris-Saclay (ComUE), 2017. http://www.theses.fr/2017SACLS134.

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Le peptide oncolytique LTX-315 a été développé comme un peptide cationique amphipathique qui tue les cellules cancéreuses et qui se révèle stimulant pour la réponse anti-cancer immune quand il est localement injecté dans des tumeurs présentent chez des souris immunocompétentes. La microscopie électronique par transmission révélées que LTX-315 a échoué à induire la condensation nucléaire apoptotique mais induit plutôt un phénotype nécrotique. Par conséquent, LTX-315 a échoué à stimuler l'activation de caspase-3, et l'inhibition des caspases par le biais de Z-VAD-fmk n'a pas été capable de réduire la mort cellulaire par LTX-315. En outre, deux inhibiteurs importants de la nécroptose, nommés necrostatin-1 et cycospotin-A, ont échoué à réduire la mort cellulaire par LTX-315. En conclusion, il semble que LTX-315 déclenche une nécrose non-régulée, qui peut contribuer à ses effets pro-inflammatoires et pro-immunitaires. Le fractionnement subcellulaire des cellules traitées par LTX-315, suivie par une quantification spectrométrique massive, a révélé que cet agent était enrichi en mitochondries. LTX-315 a causé un arrêt immédiat de la respiration mitochondriale sans aucun effet majeur de découplage. Par conséquent, LTX-315 a interrompu le réseau mitochondrial, a dissipé le potentiel mitochondrial de la membrane interne, et a causé la libération des protéines inter-membranaires mitochondriales dans le cytosol. LTX-315 était relativement inefficace dans la mitophagie stimulante. Les cellules dépourvues de deux pro-apoptotiques protéines à domaines multiples BAX et BAK, étaient moins susceptibles de mourir par LTX-315. De plus, les cellules conçues pour perdre leurs mitochondries étaient relativement résistantes à LTX-315, soulignant l'importance de cet organite pour la cytotoxicité induite par LTX-315. Au total, ces résultats soutiennent la notion que LTX-315 tue les cellules cancéreuses par sa vertue à perméabiliser les membranes mitochondriales. Nous avons observé que LTX-315 induit toutes les charactéristiques d'ICD connues. Cette conclusion a étévalidée par diverses méthodes indépendantes incluant la teinture par immunofluorence, dosage par bioluminescence, immunodosages, RT-PCRs. Quand il a été injecté dans des cancers créés, LTX-315 a causé une nécrose focale transitoirement hémorragique accompagnée d'une libération massive de HMGB1, aussi bien que l'activation de caspase-3 dans une partie des cellules. LTX-315 était au moins aussi efficace que le controle positif, l' anthracycline mitoxantrone en induisant une inflammation locale par infitration de cellules myéloïdes et de lymphocytes T. Collectivement, ces résultats appuient l'idée que LTX-315 peut induire l'ICD, expliquant sa capacité à induire des effets thérapeutiques immuno-dépendants.L'autre Lytix composé LTX-401 est un acide aminé oncolytique dérivé avec des propriétés immunogéniques potentielles. Nous démontrons que LTX-401 détruit sélectivement la strucutre du dispositif Golgi. Le fractionnement subcellulaire suivi par une détection spectométrique massive a révélé que LTX-401 a enrichi sélectivement dans le Golgi mieux que dans la mitochondrie ou dans le cytosol. Lagent Golgi-dissociant Brefeldin A a réduit la mort cellulaire par LTX-401 comme cela a partiellement inhibé la libération mitochondrial induite par LTX-401 de cytochrome C et l'activation de BAX. L'effet cytotoxique de LTX-401 a été atténué par la double suppression de BAX et BAK, comme la déplétion mitophagique forcée de la mitochondrie, déjà réfractaire à l'inhibition de caspase. LTX-401 induit toutes les caractéristiques majeures de la mort cellulaire immunogénique. En outre, les tumeurs traitées par LTX-401 ont manifesté une forte infiltration lymphoïde. Ensemble, ces résultats soutiennent l'idée que LTX-401 peut stimuler la mort immunogétique des cellules à travers un passage dans lequel LTX-401 localisé sur Golgi opère en amont de la perméabilisation de la membrane mitochondriale
The oncolytic peptide LTX-315 has been developed as an amphipathic cationic peptide that kills cancer cells and turned out to stimulate anticancer immune responses when locally injected into tumors established in immunocompetent mice. We investigated whether LTX-315 induces apoptosis or necrosis. Transmission electron microscopy or morphometric analysis of chromatin-stained tumor cells revealed that LTX-315 failed to induce apoptotic nuclear condensation and rather induced a necrotic phenotype. Accordingly, LTX-315 failed to stimulate the activation of caspase-3. Moreover, inhibition of caspases by Z-VAD-fmk was unable to reduce cell killing by LTX-315. In addition, two prominent inhibitors of necroptosis, necrostatin-1 and cyclosporin A, failed to reduce LTX-315-induced cell death. In conclusion, it appears that LTX-315 triggers unregulated necrosis, which may contribute to its pro-inflammatory and pro-immune effects. Subsequently, we investigated the putative involvement of mitochondria in the cytotoxic action of LTX-315. Subcellular fractionation of LTX-315-treated cells, followed by mass spectrometric quantification, revealed that the agent was enriched in mitochondria. LTX-315 caused an immediate arrest of mitochondrial respiration without any major uncoupling effect. Accordingly, LTX-315 disrupted the mitochondrial network, dissipated the mitochondrial inner transmembrane potential, and caused the release of mitochondrial intermembrane proteins into the cytosol. LTX-315 was relatively inefficient in stimulating mitophagy. Cells lacking the two pro-apoptotic multidomain proteins BAX and BAK, were less susceptible to LTX-315-mediated killing. Moreover, cells engineered to lose their mitochondria were relatively resistant against LTX-315, underscoring the importance of this organelle for LTX-315-mediated cytotoxicity. Altogether, these results support the notion that LTX-315 kills cancer cells by virtue of its capacity to permeabilize mitochondrial membranes. Following, we investigated whether LTX-315 may elicit the hallmarks of immunogenic cell death (ICD). Overally, we observed that LTX-315 induces all known ICD characteristics. This conclusion was validated by several independent methods including immunofluorescence staining, bioluminescence assays, immunoassays, and RT-PCRs. The injection of LTX-315 into established cancers resulted in transiently hemorrhagic focal necrosis that was accompanied by massive release of HMGB1, as well as caspase-3 activation in a fraction of the cells. LTX-315 was equal or more efficient as the positive control, the anthracycline mitoxantrone (MTX), in inducing local inflammation with infiltration by myeloid cells and T lymphocytes. Collectively, these results support the idea that LTX-315 can induce ICD, explaining its capacity to mediate immune-dependent therapeutic effects. The second Lytix compound investigated, LTX-401, is an oncolytic amino acid derivative with potential immunogenic properties. We demonstrated that LTX-401 selectively destroys the structure of the Golgi apparatus. Subcellular fractionation followed by mass spectrometric detection revealed that LTX-401 was selectively enriched in the Golgi rather than in the mitochondria or in the cytosol. The Golgi-dissociating agent Brefeldin A (BFA) reduced cell killing by LTX-401 as it partially inhibited LTX-401-induced mitochondrial release of cytochrome c and the activation of BAX. The cytotoxic effect of LTX-401 was attenuated by the double knockout of BAX and BAK, as well as the mitophagy-enforced depletion of mitochondria, yet was refractory to caspase inhibition. LTX-401 induced all major hallmarks of immunogenic cell death. Moreover, LTX-401-treated tumors manifested a strong lymphoid infiltration. Altogether, these results support the contention that LTX-401 can stimulate immunogenic cell death through a pathway in which Golgi-localized LTX-401 operates upstream of mitochondrial membrane permeabilization
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4

Goere, Diane. "Caractérisation de la mort cellulaire induite par un anticorps trifonctionnel." Thesis, Paris 11, 2013. http://www.theses.fr/2013PA11T022/document.

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Le développement d’un cancer chez un individu immunocompétent témoigne, en partie, d’un échappement tumoral au système d’immunosurveillance. Par conséquent, la restauration ou l’induction de ces mécanismes de défense anti-tumorale est une des stratégies thérapeutiques actuelles. Un des principes de l’immunothérapie est basé sur l’injection d’anticorps ayant pour cible la cellule tumorale ou les cellules effectrices de l’immunité. L’efficacité anti-tumorale de ces anticorps a été considérablement améliorée par une meilleure compréhension des modes d’action et des effets modulateurs de ces anticorps. Ainsi, afin d’optimiser l’action des effecteurs immunitaires sur les cellules tumorales, un anticorps bispécifique, trifonctionnel, le catumaxomab, capable de se lier à la molécule d'adhérence des cellules épithéliales (EpCAM) exprimée par les cellules tumorales et à l'antigène CD3 des lymphocytes T, a été développé, essentiellement en traitement intra-péritonéal des ascites néoplasiques réfractaires.L’objectif de cette étude était de déterminer les effets immunomodulateurs du catumaxomab sur des cellules néoplasiques exprimant EpCAM, à partir de deux modèles expérimentaux (allogénique et autologue), de rechercher une cytotoxicité induite par la catumaxomab, et de la caractériser, notamment en analysant la présence ou non de signaux de stress inducteurs d’une mort immunogène tels que l’exposition membranaire de la calréticuline par les cellules tumorales pré-apoptotiques, la libération d’HMGB1 et d’adénosine triphosphate (ATP) dans le milieu extra-cellulaire, responsables d’une activation des lymphocytes T.En présence de cellules EpCAM+, le catumaxomab entrainait une activation majeure des lymphocytes T (expression de CD69, CD107a, HLA-DR et PD1), stimulait une réponse inflammatoire de type Thelper 1(Th1), et provoquait la synthèse d’interféron-gamma par les lymphocytes T CD8. Le catumaxomab engageait le CD16 (FcR) des cellules monocytaires et NK. De plus, sur des modèles allogéniques, le catumaxomab, provoquait une mort cellulaire associée à la libération d’ATP et induisait une mort immunogène après pré-incubation dans de l’oxaliplatine.Par conséquent, le catumaxomab permet de moduler l’environnement immunitaire dans les ascites néoplasiques, et de convertir une inflammation chronique et immunosuppressive (Th2) en une inflammation aigüe et immunogène (Th1). En revanche, dans ces conditions, l’administration seule de catumaxomab ne semble pas déclencher de mort immunogène.Différents moyens pourraient permettre d’améliorer la cytotoxicité de cet anticorps bispécifique : (1) le combiner avec un agent anti-néoplasique tel que l’oxaliplatine afin de promouvoir une mort immunogène, (2) affiner son action sur le CD3 des lymphocytes en modifiant sa configuration spatiale (anticorps BiTE), (3) amplifier son affinité pour le récepteur Fcdes cellules accessoires (Fc défucosylé), (4) augmenter sa cytotoxicité en modifiant la cible dirigée contre la molécule du système immunitaire (anti-PD-1…). Enfin, l’utilisation clinique pourrait être facilitée en humanisant cet anticorps chimérique murin afin d’éviter la formation d’anticorps anti-murins, dirigés contre le catumaxomab.Un essai thérapeutique de phase II dont le but est d’évaluer l’efficacité du catumaxomab intrapéritonéal après chirurgie de cytoréduction complète d’une carcinose gastrique, chez des patients ayant reçu en préopératoire une chimiothérapie systémique à base d’oxaliplatine vient de débuter. Au cours de cette étude, nous allons valider la capacité du catumaxomab 1) à induire un stress cellulaire immunogène et la mort des cellules cancéreuses, 2) à modifier la polarisation des cellules effectrices vers une maladie inflammatoire Th1, 3) à promouvoir l'expression des molécules de costimulation et TRAIL sur les cellules NK et monocytes, et corréler ces biomarqueurs immunitaires à l’efficacité du traitement
The development of cancer in an immunocompetent individual reflects, in part, a tumor escape from the immunosurveillance. The tumor escape is a complex, multifactorial, in which tumor cells will evade the defense mechanisms of the host by changing their microenvironment. Therefore, restoration or induction of these defense mechanisms is one of the therapeutic strategies against cancer. One of the principles of immunotherapy is based on the injection of antibodies that target tumor cells or effector cells of immunity. The anti-tumor efficacy of these antibodies has been greatly improved by a better understanding of modes of action and modulatory effects of these antibodies.Thus, to optimize the action of immune effectors to tumor cells, a bispecific antibody, trifunctional: catumaxomab, capable of binding to the adhesion molecule of the epithelial cells (EpCAM), expressed by tumor cells and the CD3 antigen of T cells, has been developed mainly in intraperitoneal treatment of refractory malignant ascites.The objective of this study was to determine the immunomodulatory effects of catumaxomab on tumoral cells expressing EpCAM, from two experimental models (allogeneic and autologous), evaluate and characterize cytotoxicity induced by catumaxomab, and analyze the presence of stress signals inducing immunogenic cell death such as membrane exposure of calreticulin by pre-apoptotic tumor cells, release of HMGB1 and of adenosine triphosphate (ATP) in the extracellular medium, inducing a T cell activation.In the presence of EpCAM + cells, catumaxomab induced a major the activation of T cells (expression of CD69, CD107a, HLA-DR and PD1), stimulated an inflammatory response Thelper type 1 (Th1) and the synthesis of interferon-gamma by CD8 T cells. Catumaxomab committed CD16 NK cells and monocytes. More, in models allogeneic catumaxomab, caused cell death associated with ATP release and induced an immunogenic cell death after pre-incubation of oxaliplatin.Therefore, catumaxomab modulates the immune environment in malignant ascites, and convert chronic and immunosuppressive inflammation (Th2) in acute and immunogenic inflammation (Th1). However, in these conditions, catumaxomab alone does not seem to trigger immunogenic cell death.the cytotoxicity of this bispecific antibody could be enhance by different techniques: (1) combining with chemotherapy such as oxaliplatin to promote immunogenic cell death, (2) refining its action on CD3 lymphocytes by changing its spatial configuration (BiTE antibody), (3) increasing its affinity for the FcR of accessory cells (Fc aglycosylated), (4) increasing its cytotoxicity by changing the target directed against the immune molecule (anti-PD-1 ...). Finally, the clinical use could be facilitated by this humanizing murine chimeric antibody to prevent the formation of anti-murine antibodies directed against catumaxomab.A phase II clinical trial aimed to evaluate the efficacy of intraperitoneal catumaxomab after complete cytoreductive surgery of gastric carcinomatosis in patients who received preoperative systemic chemotherapy with oxaliplatin have just started. In this study, we will validate the ability of catumaxomab 1) to induce immunogenic cell stress and death of cancer cells, 2) to change the polarization of effector cells to Th1 inflammatory disease, 3) to promote the expression of costimulatory molecules and TRAIL on NK cells and monocytes, and we will correlate these immune biomarkers to treatment efficacy
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Schlemmer, Frédéric. "Mécanismes de la chimiothérapie immunogène." Thesis, Paris 11, 2013. http://www.theses.fr/2013PA11T075.

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L’amélioration constante du pronostic des pathologies cancéreuses est le fruit des progrès réalisés dans leur prévention, leur dépistage, leur diagnostic et leur traitement. Malgré l’avènement récent des thérapies ciblées, la chimiothérapie conventionnelle reste souvent le seul recours pour des patients atteints de cancer non opérable ou non éligibles pour ces thérapeutiques novatrices. Certaines chimiothérapies conventionnelles (anthracyclines et oxaliplatine notamment) ont la capacité d’entrainer une mort des cellules tumorales dont les caractéristiques permettent d’induire une réponse immunitaire antitumorale efficace. Cette réponse immunitaire antitumorale spécifique agirait en synergie avec l’effet cytotoxique direct de ces drogues, participant ainsi à leur efficacité. La réponse immunitaire antitumorale induite par la chimiothérapie dépend de plusieurs mécanismes moléculaires et cellulaires clefs identifiés récemment. L’induction d’un stress du réticulum endoplasmique (RE) est à l’origine de l’exposition d’une protéine chaperonne résidente du RE, la calréticuline (CRT), à la surface des cellules mourantes, servant alors de signal de phagocytose pour les cellules dendritiques. La libération dans le milieu extracellulaire de signaux de danger est également essentielle : la protéine nucléaire High Mobility Group Box 1 (HMGB1) sert ainsi de ligand pour le Toll-like récepteur 4 (TLR4), présent à la surface des cellules dendritiques et son activation favorise l’apprêtement et la présentation des antigènes tumoraux aux lymphocytes T cytotoxiques. L’adénosine-5'-triphosphate (ATP) est également libéré par les cellules tumorales, entrainant l’activation des récepteurs purinergiques P2RX7 présents à la surface des cellules dendritiques, activant l’inflammasome NLRP3 et entrainant la libération d’IL-1 par les cellules dendritiques, favorisant alors l’orientation de la réponse immunitaire vers une réponse de type TH1 et la production d’interféron  par les lymphocytes T cytotoxiques. Dans ce travail, nous avons cherché à comparer la capacité de deux drogues issues d’une même classe de chimiothérapie, les sels de platine, à induire une mort cellulaire immunogène des cellules tumorales. Grace à des expériences in vitro et in vivo (modèles murins de vaccination antitumorale et de chimiothérapie sur tumeurs établies), nous avons pu montrer que l’oxaliplatine (OXP), contrairement au cisplatine (CDDP), avait la capacité d’induire une mort immunogène des cellules de cancer colique et que cette différence intra-classe dépendait de la capacité respective de ces deux drogues à entrainer un des phénomènes clés de l’induction d’une mort cellulaire immunogène, l’exposition de la CRT à la surface des cellules tumorales mourantes. Nous avons également pu montrer que l’induction d’une mort cellulaire immunogène des cellules de cancer colique par l’oxaliplatine avait une relevance clinique chez l’homme, l’existence d’un polymorphisme perte-de-fonction du gène tlr4 affectant le pronostic (survie sans progression) de patients traités par chimiothérapie pour un cancer colique métastatique. Par la suite, nous avons mis au point des biosondes permettant d’étudier à grande échelle, à l’aide d’une plateforme de vidéo-microscopie automatisée, la capacité de différentes drogues à induire les différents phénomènes clefs de la mort cellulaire immunogène des cellules tumorales (exposition de la CRT, libération d’HMGB1 et d’ATP). Nous avons ainsi pu montrer que la correction pharmaceutique du défaut d’activation d’un stress du réticulum endoplasmique par le cisplatine permettait de restaurer l’immunogénicité de la mort cellulaire induite par cette chimiothérapie. Ces résultats ouvrent la voie à la découverte de nouvelles molécules susceptibles, à elles seules ou en association à d’autres thérapies connues, d’améliorer le pronostic des néoplasies
The steady improvement of cancer prognosis is the result of progress in cancer prevention, screening, diagnosis and treatment. Despite the recent advent of targeted therapies, conventional chemotherapy often remains the only solution for patients with non-operable cancer or not eligible for these novel therapies.Some conventional chemotherapy (including anthracyclines and oxaliplatin) has the ability to cause tumor cells death with characteristics able to induce an effective antitumor immune response. This specific antitumor immune response would be synergistic with the direct cytotoxic effect of these drugs and contribute to their efficacy. The antitumor immune response induced by chemotherapy depends on several key cellular and molecular mechanisms recently identified. The induction of an endoplasmic reticulum (ER) stress is necessary for the exposure of calreticulin (CRT), an ER-resident chaperone protein, on the surface of dying cells, then acting as a phagocytosis signal for dendritic cells. Release of danger signals into the extracellular medium is also essential. The nuclear protein High Mobility Group Box 1 (HMGB1) is a ligand of the Toll-like receptor 4 (TLR4) on the surface of dendritic cells. TLR4 activation promotes the processing of tumor antigens and their presentation to cytotoxic T lymphocytes. Adenosine-5'-triphosphate (ATP) is also released by tumor cells, leading to the activation of the purinergic receptors P2RX7 expressed on the surface of dendritic cells, activating the NLRP3 inflammasome and causing the release of IL-1β by dendritic cells, while promoting the orientation of the immune response towards a TH1 response and the production of γ-interferon by cytotoxic T lymphocytes.In this work, we aimed to compare the ability of two drugs of a same class of chemotherapy, the platinum derivates oxaliplatin (OXP) and cisplatin (CDDP), to induce immunogenic death of tumor cells. Thanks to in vitro and in vivo experiments (models of tumor vaccination and chemotherapy on established tumors in mice), we showed that OXP, in contrast to CDDP, has the ability to induce immunogenic death of colon cancer cells. This intra-class difference depends on the ability of each drug to cause one of the key phenomena of immunogenic cell death: the induction of the exposure of the CRT to the surface of dying tumor cells. We could also show that the induction of immunogenic death of colon cancer cells by OXP had clinical relevance in humans. Indeed, the existence of a loss-of-function polymorphism of tlr4 affects the prognosis (PFS) of patients treated with OXP-based chemotherapy regimen for a metastatic colorectal cancer. Subsequently, we developed biosensors to study the ability of different drugs to induce key phenomena of cell death immunogen tumor cells (CRT exposure, HMGB1 and ATP release) using high-content screening by an automated video-microscopy platform. We showed that a pharmaceutical correction of the inability of cisplatin to induce an endoplasmic reticulum stress could restore the immunogenicity of cisplatin-induced tumor cell death. These results open the way to the discovery of new molecules that, alone or in combination with other known therapies, could improve the prognosis of cancer
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Ko, Adrien. "Impact de l’autophagie sur la radiosensibilité tumorale." Thesis, Paris 11, 2013. http://www.theses.fr/2013PA11T074.

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Les données existantes sur le rôle de l’autophagie dans la mort cellulaire radio-induite sont controversées et proviennent d’études pour lesquelles sont utilisées des drogues : l’action se produit donc de manière indirecte. Certains suggèrent que l’induction combinée de l’apoptose et de l’autophagie améliore le traitement par radiations ionisantes. D’autres indiquent que l’induction de l’autophagie favoriserait la radiorésistance des cellules tumorales et que l’utilisation d’inhibiteurs de l’autophagie augmenterait la réponse des tumeurs aux radiations ionisantes. L'autophagie, ou «self-eating», est un processus cellulaire activé par diverses conditions de stress, par lequel les cellules peuvent dégrader les protéines et les organites. Nous avons au cours de cette étude cherché à déterminer le rôle de l'autophagie dans la mort cellulaire radio-induite. Selon nos observations, l'autophagie est nécessaire pour la libération de l'ATP après un traitement par radiothérapie: en effet, le knockdown de gènes essentiels à l'autophagie limite la sécrétion d'ATP. Nous avons également constaté que des cellules déficientes pour l'autophagie traitées par radiothérapie sont incapables d’immuniser des souris contre une injection de cellules vivantes. En outre, les tumeurs déficientes pour l’autophagie répondent moins bien à un traitement par radiations ionisantes dans des souris immunocompétentes et continuent à proliférer, contrairement aux tumeurs “wild-type”. De plus, nous avons montré que les cellules déficientes pour l'autophagie ne sont pas en mesure de recruter des cellules dendritiques dans le lit tumoral. A l'inverse, l'inhibition des enzymes de dégradation de l’ATP extracellulaire accroît les concentrations d'ATP dans les tumeurs déficientes pour l'autophagie, ce qui rétablit le recrutement des cellules immunitaires dans le lit tumoral et restaure la réponse à la radiothérapie des cancers déficients pour l'autophagie. Ainsi, cette étude a montré l'importance de l'autophagie dans la réponse anti-tumorale spécifique, après traitement par radiations ionisantes. Ces résultats ouvrent de nouvelles perspectives pour comprendre la mort cellulaire radio-induite. Il reste cependant à découvrir les mécanismes moléculaires sous-jacents pour développer de nouvelles thérapies ciblées qui amélioreront l’efficacité de la radiothérapie
Most of the available data on autophagy and tumor response to IR comes from indirect conclusions after concomitant drug-IR exposure. Some authors suggest that concurrent induction of apoptosis and autophagy enhances radiation therapy. Oppositely, others indicate that the induction of autophagy contributes to the radioresistance of tumor cells and suggest that autophagy inhibitors may be employed to increase the sensitivity radioresistant tumors cells to ionizing radiation. Autophagy literally ‘self-eating’ is a cellular process activated in response to various conditions of cellular stress, whereby cells can liberate energy resources via the degradation of proteins and organelles. In this project we aimed to determine the potential role of autophagy in IR –induced cell death. We found that autophagy is required for the release of ATP in response to radiotherapy, as we observed that the knockdown of essential autophagy-related genes abolished its secretion. Furthermore, autophagy deficient tumors growing on immunocompetent mice did not respond to radiotherapy and continued proliferating in contrast to autophagy proficient tumors. We showed that autophagy deficient cells were neither able to recruit DCs into the tumor bed. Conversely, the inhibition of extracellular ATP degrading enzymes increased extracellular ATP concentrations in autophagy deficient tumors, which reestablished the recruitment of immune cells into the tumor bed, and restored radiotherapeutic responses in autophagy-deficient cancers.Altogether, this study showed the importance of autophagy in tumor-specific immune response after radiotherapy. Thus giving new insights into the concept of IR-induced cell death. However, there is still much that is unknown about molecular mechanisms that undergo IR-induced cell death. Understand these molecular mechanisms will help to develop new targeted therapies that will improve the effectiveness of radiotherapy
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Parney, Ian Frederick. "Human glioma immunology and immunogene therapy." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape8/PQDD_0003/NQ39580.pdf.

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Kjerrström, Zuber Anne. "Enhancement of HIV-1 DNA immunogens /." Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-304-x.

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Ljungberg, Karl. "Variable viral genes as genetic immunogens /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-399-6/.

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Karras, Marianna. "Evaluation of immunogen delivery by insects." Thesis, Imperial College London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.409270.

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Books on the topic "Immunogeni"

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Koprowski, Hilary, and Fritz Melchers, eds. Peptides as Immunogens. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71440-5.

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Lawson, David Alexander. Identification of immunogenic proteins of litomosoides carinii (Nematoda, Filarioidea). Salford: University of Salford, 1988.

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Peptides as Immunogens. Berlin: Springer-Verlag, 1986.

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Melchers, Fritz, and Hilary Koprowski. Peptides As Immunogens. Springer London, Limited, 2012.

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Melchers, Fritz, and Hilary Koprowski. Peptides As Immunogens. Springer, 2011.

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Kitazawa, Haruki, Susana Alvarez, and Julio Villena. Probiotics: Immunobiotics and Immunogenics. Taylor & Francis Group, 2013.

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Kitazawa, Haruki, Susana Alvarez, and Julio Villena. Probiotics: Immunobiotics and Immunogenics. Taylor & Francis Group, 2013.

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Probiotics immunobiotics and immunogenics. CRC Press, 2014.

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Bruce, Simon. Probiotics: Immunobiotics and Immunogenics. Murphy & Moore Publishing, 2022.

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Kitazawa, Haruki. Probiotics: Immunobiotics and Immunogenics. Taylor & Francis Group, 2013.

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Book chapters on the topic "Immunogeni"

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Gooch, Jan W. "Immunogenic." In Encyclopedic Dictionary of Polymers, 901. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_13996.

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Raghava, Gajendra. "Immunogen." In Encyclopedia of Systems Biology, 997. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-9863-7_784.

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Gooch, Jan W. "Immunogen." In Encyclopedic Dictionary of Polymers, 900. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_13995.

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Lichtor, Terry, and Roberta P. Glick. "Immunogene Therapy." In Advances in Experimental Medicine and Biology, 151–65. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3146-6_12.

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Pitt, Jonathan M., Guido Kroemer, and Laurence Zitvogel. "Immunogenic and Non-immunogenic Cell Death in the Tumor Microenvironment." In Advances in Experimental Medicine and Biology, 65–79. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-67577-0_5.

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Bolchi, Angelo, Elena Canali, Andrea Santoni, Gloria Spagnoli, Daniele Viarisio, Rosita Accardi, Massimo Tommasino, Martin Müller, and Simone Ottonello. "Thioredoxin-Displayed Multipeptide Immunogens." In Methods in Molecular Biology, 137–51. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2999-3_14.

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Goretzki, P. E. "Autogene und immunogene Hyperthyreose." In Deutsche Gesellschaft für Chirurgie, 951. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-48163-5_197.

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Brown, F. "Synthetic Peptides as Immunogens." In New Vaccines and Chemotherapy, 93–106. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4757-9268-3_9.

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Milligan, Gregg N. "Adjuvants: Making Vaccines Immunogenic." In Vaccinology, 93–108. Oxford, UK: John Wiley & Sons, Ltd, 2014. http://dx.doi.org/10.1002/9781118638033.ch6.

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Pulakkat, Sreeranjini, and Vandana Patravale. "Immunogene Therapy in Cancer." In Biotechnology in the Modern Medicinal System, 153–82. Boca Raton: Apple Academic Press, 2021. http://dx.doi.org/10.1201/9781003129783-6.

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Conference papers on the topic "Immunogeni"

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Hamza, Shaimaa, Ekaterina Evgenevna Garanina, Ekaterina Vladimirovna Martynova, Maria Ivanovna Markelova, Jurij Nikolaevich Davidyuk, Venera Gusmanovna Shakirova, and Svetlana Francevna Khaiboullina. "Antibody Immune Responses to SARS-CoV-2 Peptides in COVID-19 Convalescent Patients." In All-Russian scientific conference with International Participation. Publishing house Sreda, 2022. http://dx.doi.org/10.31483/r-102484.

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Identifying immunogenic targets of SARS-CoV-2 is essential to develop novel treatments. The authors of the article studied humoral immune responses to spike (S) and nucleocapsid (N) SARS-CoV-2 proteins in serum from convalescent COVID-19 patients from Tatarstan, Russia. Multiple SARS-CoV-2 peptides were identified as reacting with convalescent COVID-19 serum. In addition, age and gender associated differences in the reactivity to S and N protein peptides were identified. Changing pattern of immunogenic peptide reactivity in COVID-19 serum based on age and gender was demonstrated. These data highlight how humoral immune responses to some of these peptides could contribute to SARS-CoV-2 pathogenesis.
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Schneider, C. H. "Peptides as immunogens and allergens." In Future Aspect in Peptide Chemistry - Ringberg Conference. Prague: Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, 1999. http://dx.doi.org/10.1135/css199901095.

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Chizenga, Elvin Peter, and Heidi Abrahamse. "Enhancing Photodynamic Therapy of Cancer by Intracellular Delivery of Photosensitizer." In Frontiers in Optics. Washington, D.C.: Optica Publishing Group, 2022. http://dx.doi.org/10.1364/fio.2022.jtu5a.67.

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Immunogenic proteins in cancer are relevant targets for drug delivery. A multifunctional photo-activating compound directed to such proteins was developed for Photodynamic Therapy of Human Papillomavirus-transformed cancer cells. Selective binding increased therapeutic efficacy by two-folds.
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Kanaya, Nobuhiko, Shinji Kuroda, Toshiaki Morihiro, Yoshihiko Kakiuchi, Tetsushi Kubota, Satoru Kakiuchi, Masahiko Nishizaki, et al. "Abstract 2744: Telomelysin-induced immunogenic cell death synergizes with anti-PD-1 antibody in non-immunogenic gastrointestinal tumors." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-2744.

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Gardai, Shyra J., Angela Epp, and Che-Leung Law. "Abstract 2469: Brentuximab vedotin-mediated immunogenic cell death." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-2469.

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Liao, Jun, Erinn M. Joyce, Hugh L. Jones, Mina Tahai, Ali Borazjani, W. David Merryman, and Michael S. Sacks. "The Intrinsic Durability of Aortic Valve ECM in Absence of Cellular Maintenance." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-193110.

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In the last two decades, decellularized native aortic valve (AV) has been investigated as tissue engineered heart valve (TEHV) replacements due to their potential to develop into a viable valve.[1] Decellularization removes major immunogenic cellular components. After repopulated with recipient’s cells, TEHV can be readily used because of the necessary functional design.[2] However, several problems with this approach have been identified, such as insufficient cell infiltration, mechanical deterioration, formation of fibrous sheath on implantation, and reduced orifice area after surgery.[3]
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"Lcr1 Immunogen Sequencing and Anti-Leishmaniasis Vaccine Producing." In AEBMS-2017, ICCET-2017, BBMPS-17, UPACEE-17, LHESS-17, TBFIS-2017, IC4E-2017, AMLIS-2017 & BEFM-2017. Higher Education and Innovation Group (HEAIG), 2018. http://dx.doi.org/10.15242/heaig.c1217229.

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Hodge, James W., Charlie T. Garnett, Benedetto Farsaci, Claudia Palena, Kwong-Yok Tsang, Soldano Ferrone, and Sofia R. Gameiro. "Abstract 1676: Chemotherapy-induced immunogenic modulation of tumor cells enhances killing by cytotoxic T lymphocytes and is distinct from immunogenic cell death." In 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.am2013-1676.

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Sheridan, W. S., O. Grant, A. Lopez-Noriega, G. P. Duffy, and B. P. Murphy. "Towards a Clinically Applicable Tissue Engineered Vascular Graft." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14457.

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Decellularized arterial tissue has shown promising use as a scaffold for vascular tissue replacement; similar structural and functional characteristics to the native tissue are maintained and these scaffolds are non-thrombogenic, non immunogenic with the ability to remodel and grow in vivo[1]. However, there still remains a number of limiting factors in clinically translating these scaffolds. Namely, producing a range of geometries to accommodate a large patient cohort within clinically feasible manufacturing times and costs. Furthermore, these scaffolds must be suitable for long term preservation to produce a reasonable shelf life and be capable of undergoing standard sterilization techniques.
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Tan, Conge, Miqu Wang, Weijun Ding, Weihong Li, and Louxin Zhang. "Expression Profile of Immunogenes in Cold Constitution." In 2007 1st International Conference on Bioinformatics and Biomedical Engineering. IEEE, 2007. http://dx.doi.org/10.1109/icbbe.2007.96.

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Reports on the topic "Immunogeni"

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Johnston, Robert E. Attenuated VEE Vaccine Vectors Expressing HIV Immunogens. Fort Belvoir, VA: Defense Technical Information Center, September 1995. http://dx.doi.org/10.21236/ada307632.

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Spencer, David M., and Kevin M. Slawin. Regulated Apoptosis and Immunogene Therapy for Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, April 2006. http://dx.doi.org/10.21236/ada456011.

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Fournier, Maurille J., and Thomas L. Mason. Structure and Expression of Genes for Flavivirus Immunogens. Fort Belvoir, VA: Defense Technical Information Center, January 1992. http://dx.doi.org/10.21236/ada252662.

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Haynes, Barton F. Structural and Functional Studies of Experimental HIV Synthetic Peptide Immunogens. Fort Belvoir, VA: Defense Technical Information Center, October 1997. http://dx.doi.org/10.21236/ada333309.

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Paget, Christophe, Helene Duret, and Mark J. Smyth. Role of Natural Killer T Cells In Immunogenic Chemotherapy for Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2012. http://dx.doi.org/10.21236/ada571626.

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Paget, Christophe, Helene Duret, and Mark J. Smyth. Role of Natural Killer T Cells in Immunogenic Chemotherapy for Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2013. http://dx.doi.org/10.21236/ada595285.

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Markovic, Dubravka, and Edward P. Cohen. Treatment of Breast Cancer with Immunogenic Cells Transfected with DNA from Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, July 2001. http://dx.doi.org/10.21236/ada396744.

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Chedid, Louis. Construction of Synthetic Immunogens in View of Developing Orally-Active Anti-Enterotoxigenic E. coli Vaccines. Fort Belvoir, VA: Defense Technical Information Center, May 1989. http://dx.doi.org/10.21236/ada223644.

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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.

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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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Romoser, William S. The Influence of Antibodies to Selected Mosquito Immunogens on Mosquitoes Following Ingestion of Blood from an Immune Vertebrate Host. Fort Belvoir, VA: Defense Technical Information Center, August 1992. http://dx.doi.org/10.21236/ada254789.

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