Gotowe bibliografie tematyczne / Humoral immunity

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Gotowa bibliografia na temat „Humoral immunity”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 29 stycznia 2023

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Artykuły w czasopismach na temat "Humoral immunity"

Kiilstra, Aize. "Ocular humoral immunity". Experimental Eye Research 55 (wrzesień 1992): 29. http://dx.doi.org/10.1016/0014-4835(92)90311-f.

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Dunn, Peter E. "Humoral Immunity in Insects". BioScience 40, nr 10 (listopad 1990): 738–44. http://dx.doi.org/10.2307/1311506.

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STEAD, A., J. G. DOUGLAS, C. J. BROADFOOT, E. R. KAMINSKI i R. HERRIOT. "Humoral immunity and bronchiectasis". Clinical & Experimental Immunology 130, nr 2 (17.10.2002): 325–30. http://dx.doi.org/10.1046/j.1365-2249.2002.01974.x.

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Virella, Gabriel, i Maria F. Lopes-Virella. "Humoral immunity and atherosclerosis". Nature Medicine 9, nr 3 (1.03.2003): 243–44. http://dx.doi.org/10.1038/nm0303-243.

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CHALLACOMBE, S. J. "Assessing mucosal humoral immunity". Clinical & Experimental Immunology 100, nr 2 (28.06.2008): 181–82. http://dx.doi.org/10.1111/j.1365-2249.1995.tb03649.x.

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Carroll, Michael C. "Complement and humoral immunity". Vaccine 26 (grudzień 2008): I28—I33. http://dx.doi.org/10.1016/j.vaccine.2008.11.022.

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Chavarria-Smith, Joseph, Wouter L. W. Hazenbos i Menno van Lookeren Campagne. "Humoral immunity goes hormonal". Nature Immunology 19, nr 10 (19.09.2018): 1044–46. http://dx.doi.org/10.1038/s41590-018-0216-x.

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Koch, Cody A., Zain I. Khalpey i Jeffrey L. Platt. "Humoral immunity in xenotransplantation". Current Opinion in Organ Transplantation 9, nr 2 (czerwiec 2004): 170–75. http://dx.doi.org/10.1097/01.mot.0000127677.16900.27.

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Jacobs, Ashley, i Robert John Wilkinson. "Humoral immunity in tuberculosis". European Journal of Immunology 45, nr 3 (marzec 2015): 647–49. http://dx.doi.org/10.1002/eji.201570034.

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Paganelli, R., E. Scala, I. Quinti i I. J. Ansotegui. "Humoral immunity in aging". Aging Clinical and Experimental Research 6, nr 3 (czerwiec 1994): 143–50. http://dx.doi.org/10.1007/bf03324229.

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Rozprawy doktorskie na temat "Humoral immunity"

Nohr, Carl William. "Humoral immunity in surgical patients". Thesis, McGill University, 1988. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=75969.

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Humoral immune function was studied in surgical patients. The antibody response to vaccination with a protein antigen, tetanus toxoid (TT), was reduced among all patients, especially those with reduced delayed type hypersensitivity (DTH) and increased degree of physiological derangement. The antibody response to a polysaccharide antigen, pneumococcal polysaccharide (PPS), was normal. In trauma patients, the antibody response to TT was normal. The in vitro production of specific and total immunoglobulin (Ig) by blood mononuclear cells was studied. Patients that failed to produce a serum antibody response to TT also failed to produce anti-TT in vitro. Anti-PPS production was normal. More total Ig was produced by patients, especially those with reduced DTH responses. Some patients showed a reduction, rather than the normal increase, in Ig synthesis with mitogen stimulation. These data show evidence of humoral immune deficiency to protein antigens, and in vivo activation of the B cell system.

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Cassis, Linda 1977. "Role of progranulin in humoral immunity". Doctoral thesis, Universitat Pompeu Fabra, 2015. http://hdl.handle.net/10803/398398.

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Human spleen is continually exposed to blood-borne antigens derived from autologous apoptotic cells and commensal bacteria. This chronic stimulation of the marginal zone (MZ) results in the generation of a steady-state antibody response that occurs under non-inflammatory conditions. Immunoregulatory signals, still poorly understood, are required to avoid continuous inflammation. Our group identified a population of splenic neutrophils called B cell-helper neutrophils (NBH cells) that contribute to the induction of steady-state antibody responses in the MZ1. NBH cells express B cell-activating and immunoregulatory factors, including progranulin (PGRN). PGRN is an anti-inflammatory protein highly expressed at sites constantly exposed to antigens. It was shown to regulate several processes, including embryogenesis, neuronal survival, and wound repair. However, the role of PGRN in the immune response is still largely unknown. Here we show that PGRN actively participates in the pre-immune and post-immune responses against splenic microbial antigens, regulating the frequency and/or function of innate and adaptive immune cells such as neutrophils, dendritic cells, T and B cells. These findings suggest that PGRN functions as an endogenous adjuvant that may facilitate the development of novel strategies for modulating protective immune responses against invading pathogens.
El bazo humano está continuamente expuesto a antígenos provenientes de la sangre derivados de células apoptóticas autólogas y bacterias comensales. Esta estimulación crónica de la zona marginal (ZM) resulta en la generación de una respuesta de anticuerpos que se produce de forma fisiológica bajo condiciones no inflamatorias. Para evitar la inflamación continua, se requieren señales inmunorreguladoras, todavía poco conocidas. Nuestro grupo identificó una población de neutrófilos esplénicos llamada neutrófilos ayudantes de células B (células NBH)1 que contribuyen a la inducción de anticuerpos en la ZM en condiciones fisiológicas. Las células NBH expresan factores activadores de las células B y factores inmunorreguladores, incluyendo progranulina (PGRN). PGRN es una proteína antiinflamatoria altamente expresada en lugares constantemente expuestos a antígenos. Regula varios procesos, incluyendo la embriogénesis, la supervivencia neuronal, y la reparación de heridas. Sin embargo, el papel de PGRN en la respuesta inmune sigue siendo en gran medida desconocido. En este estudio demostramos que PGRN participa activamente en las respuestas pre- y post-inmunes contra antígenos microbianos en el bazo, regulando la frecuencia y / o la función de células inmunitarias innatas y adaptativas como neutrófilos, células dendríticas, células T y B. Estos hallazgos sugieren que PGRN actúa como un adyuvante endógeno que puede facilitar el desarrollo de nuevas estrategias para modular la respuesta inmunitaria protectora contra patógenos invasores.

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Rydyznski, Carolyn E. "Natural Killer Cell Regulation of Humoral Immunity". University of Cincinnati / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1535377157934852.

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Berkeley, Robert Anthony. "Immune cell carriers and humoral immunity in oncolytic virotherapy". Thesis, University of Leeds, 2018. http://etheses.whiterose.ac.uk/20532/.

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Oncolytic viruses (OV) represent an emerging modality in cancer therapy. Antiviral immunity is currently viewed as a barrier to systemic OV efficacy. Approaches have been taken to promote OV activity by attenuating virus-neutralising antibodies (NAb). However, the presence of NAb does not prevent intravenously administered OV, such as reovirus, reaching tumours in patients. Recent evidence suggests that NAb may in fact support virotherapy in mice by facilitating reovirus carriage upon circulating immune cells, principally monocytes. In this thesis, the applicability of these observations to the human setting is examined, modelling the loading of monocytes with reovirus in virus-immune patients. A novel in vitro cell carriage assay was employed, involving clinical trial patient-derived sera, isolated primary human monocytes, and human tumour cell lines. It was discovered that monocytes treated with fully neutralised reovirus reliably delivered the virus to kill melanoma targets. This was transferable across target cell histologies, and applicable to another OV, CVA21. Neutralised reovirus successfully accessed syngeneic melanoma flank tumours in mice. Prior murine studies suggested a role for surface Fc receptors in facilitating the antibody-dependent enhancement (ADE) of monocyte infection. A major role for Fc receptors in antibody-mediated entry of neutralised reovirus to human monocytes was confirmed. Yet no overall enhancement of virus loading or hand-off was conferred by the presence of NAb, in contrast to existing observations from mouse monocytes. Transcriptomic and secretory profiling identified discrete variations in the effects of free and neutralised reovirus upon monocyte phenotype. NAb significantly attenuated the monocyte IFN response to reovirus in vitro. However, in the presence of monocytes, reo-NAb successfully induced NK cell degranulation and killing of melanoma targets. Therefore this study identifies a mechanism by which, following neutralisation, reovirus may rely on circulating monocytes to gain tumour access, and to initiate oncolytic and/or immune-mediated tumour cell death.

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Willems, Kristen N. "Regulation of Humoral Immunity by Pim Kinases: A Dissertation". eScholarship@UMMS, 2011. https://escholarship.umassmed.edu/gsbs_diss/567.

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Pim (Provirus Integration site for Moloney murine leukemia virus) kinases are a family of three serine/threonine kinases involved in cell cycle, survival and metabolism. These kinases were first identified in malignant cells and are most often associated with their role in cancer. Their role in immunity and lymphocytes is less well known. To date, it has been shown that Pim 1 and/or Pim 2 are important for T lymphocyte survival and activation when the Akt signaling pathway is inhibited by rapamycin. In addition, our laboratory has shown that Pim 2 is critical for BLyS-mediated naive B lymphocyte survival in the presence of rapamycin. This thesis extends the role(s) for Pim 1 and/or 2 to include functions during B cell activation and the generation of immune responses. We found that during in vitro activation of purified resting splenic B cells from wild type mice with a variety of activators that use multiple signaling pathways, including the BCR, TLR and CD40 receptors, both Pim 1 and 2 kinases were induced by 48 hours post-activation, suggesting that they could play a role in B cell activation and differentiation to antibody secreting or memory B cells. Immunization of Pim 1-/-2-/- knockout mice with T cell dependent antigens showed impairment in antibody and antibody secreting cell generation as well as lack of germinal center formation clearly demonstrating an involvement of Pim 1 and/or 2 in the immune response. FACS examination of B cell populations from naive Pim 1-/-2-/- knockout mice revealed normal levels of splenic marginal zone and follicular B cells and T cells, however, decreased numbers of all peritoneal B cell populations and decreased B cells in Peyer's Patches was seen. An examination of serum antibody found in naive Pim 1-/-2-/- knockout mice showed decreased levels of natural antibody, which is likely due to loss of the peritoneal B1 cells but does not explain the significantly decreased TD immune response. To determine whether the defect was B cell intrinsic or a more complex interaction between B and T cells, we determined whether Pim 1-/-2-/- mice would respond to T cell independent, TI-1 and TI-2, antigens. Antibody production and antibody secreting cell formation were also significantly decreased in these mice supporting our notion of a B cell intrinsic defect. To further examine the B cell response problem, we attempted to establish chimeric mice using either bone marrow derived cells or fetal liver cells from WT or Pim 1-/-2-/- donors so that the B cells were derived from Pim 1-/-2-/- mice and the T cells would be WT. Unfortunately, we were not able to consistently engraft and develop mature Pim 1-/-2-/- B cells, which indicate that there is a stem cell defect in these knockout mice that requires further investigation. Because one of the major failures in activated Pim 1-/-2-/- B cells is the generation of antibody secreting cells, an analysis of the expression of transcription factors IRF-4 and BLIMP-1, known to play a role in this process was carried out. Although IRF-4 induction was not affected by the loss of Pim 1 and 2, the number of cells able to increase BLIMP-1 expression was significantly decreased, revealing a partial block in the generation of ASCs. Taken together the data presented in this thesis reveals a new and critical role for Pim 1 and 2 kinases in the humoral immune response.

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Bruns, Nicholas Joseph. "Humoral and cell-mediated immunity in vitamin A-deficient lambs". Diss., Virginia Polytechnic Institute and State University, 1988. http://hdl.handle.net/10919/53919.

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Antigen-specific and polyclonal serum immunoglobulin G (IgG) concentrations were measured in control (Con), vitamin A-deficient (A-def), and vitamin A-repleted (A-rep) lambs. In Trial, I ewe lambs were injected with primary and secondary antigenic challenges of ovalbumin (1mg) and lysozyme (.1mg). The A-def lambs were then repleted with vitamin A and all lambs were injected with primary and secondary antigenic challenges of human gamma globulin (HGG) (.1mg). In Trial II Con and A-def wether lambs were given primary and secondary antigenic challenges of ovalbumin (20μg). Half of the A-def lambs were then repleted with vitamin A. All lambs were subsequently given a primary and secondary challenge of HGG (20 μg). Spleen wt were similar for all treatments in Trial I while A-def V lambs in Trial II had greater spleen wt (P<.01) than Con or A-rep lambs. Polyclonal serum IgG concentrations were unaffected by treatment in Trial I while in Trial II concentrations were greater (P<.05) in the A-def lambs during the HGG challenge period. Antigen-specific IgG concentrations in both trials tended to be greater in the Con lambs towards the end of both the ovalbumin (Trial I and II) and lysozyme (Trial I) challenge periods. Control and A-rep lambs in Trial I responded similarly to the HGG challenges. In Trial II both the A-def and A-rep lambs had lower (P<.10) HGG specific serum IgG concentrations on the last 3 wk of the HGG challenge period as compared to A-def lambs. Humoral immune function appears to be impaired in A-def lambs and a 2-wk repletion period was not sufficient in this study to restore humoral immune function to normal levels.
Ph. D.

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Sallam, Jamal A. "Intestinal humoral immunity in man : IgA and anti-salmonella antibodies". Thesis, University of Edinburgh, 1995. http://hdl.handle.net/1842/20766.

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Studies of gut immunity must be carried out on intestinal fluid and jejunal biopsies. Recent work from Edinburgh has shown that the use of Whole Gut Lavage (WGL) technique is a non-invasive, direct and reliable method of obtaining intestinal fluids. My thesis describes the use of WGL technique in a variety of studies on gastro-intestinal mucosal immunity. The effect of the newly licensed oral live typhoid vaccine Ty21a on gut immunity was investigated in a group of 22 healthy British volunteers. Later on, the intestinal immune responses to naturally acquired Salmonella infection were investigated in a group of patients who had had the infection within the preceding 12 months. Results obtained in these studies were compared with results obtained from healthy individuals, patients with inflammatory bowel disease (IBD) and African children from Sierra Leone. I investigated further the effect of heavy smoking and non-smoking in healthy volunteers on gut immunity and the effect of administration of the live oral vaccine Ty21a on the intestinal mucosal immune responses of smokers and non-smokers. I also studied agglutinating antibodies in WGL fluids and sera. Patients with a variety of GI diseases and patients who had had Salmonella infection were tested against a panel of 11 Salmonella antigens using a modified Widal test in microtitration plates. In the course of the above studies, I found that there were patients who had very low or absent intestinal IgA but had normal levels of IgA in the serum. Therefore, I investigated further this phenomenon by counting plasma cells in the lamina propria of intestinal biopsies from patients with "intestinal IgA deficiency" and normal controls using image analysis.

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Casas, Rosaura. "Transfer of humoral immunity from the mother to her off-spring /". Linköping : Univ, 2001. http://www.bibl.liu.se/liupubl/disp/disp2001/med692s.pdf.

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Lucin, Kurt M. "Mechanisms of impaired humoral immunity after high thoracic spinal cord injury". Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1186411177.

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Titanji, Kehmia. "Mechanisms underlying impaired humoral immunity in primary and chronic HIV-1 infection /". Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-728-6/.

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Książki na temat "Humoral immunity"

1928-, Gupta A. P., red. Hemocytic and humoral immunity in arthropods. New York: Wiley, 1986.

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Giuseppe, Remuzzi, red. Humoral immunity in kidney transplantation: What clinicians need to know. Basel: Karger, 2009.

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Karcher, D. Humoral Immunity in Neurological Diseases. Springer, 2014.

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Karcher, D. Humoral Immunity in Neurological Diseases. Springer, 2012.

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Karcher, D. Humoral Immunity in Neurological Diseases. Springer London, Limited, 2013.

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Remuzzi, G., S. Chiaramonte, N. Perico i C. Ronco, red. Humoral Immunity in Kidney Transplantation. S. Karger AG, 2008. http://dx.doi.org/10.1159/isbn.978-3-8055-8959-8.

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M, Snapper Clifford, red. Cytokine regulation of humoral immunity: Basic and clinical aspects. Chichester: J. Wiley, 1996.

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Snapper, Clifford M. Cytokine Regulation of Humoral Immunity: Basic and Clinical Aspects. Wiley & Sons, Incorporated, John, 2008.

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Cytokine Regulation of Humoral Immunity: Basic and Clinical Aspects. Wiley, 1996.

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Valanne, Susanna, Dan Hultmark i Laura Vesala, red. Recent Advances in Drosophila Cellular and Humoral Innate Immunity. Frontiers Media SA, 2020. http://dx.doi.org/10.3389/978-2-88966-191-6.

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Części książek na temat "Humoral immunity"

Kozel, T. R., i D. M. Lupan. "Humoral Immunity". W Human and Animal Relationships, 99–115. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-662-10373-9_4.

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Mehlhorn, Heinz. "Humoral Immunity". W Encyclopedia of Parasitology, 1300. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-43978-4_4989.

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Sulentic, Courtney E. W., i Norbert E. Kaminski. "Humoral Immunity". W Encyclopedia of Immunotoxicology, 403–6. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-54596-2_707.

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Mehlhorn, Heinz. "Humoral Immunity". W Encyclopedia of Parasitology, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27769-6_4989-1.

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Gooch, Jan W. "Humoral Immunity". W Encyclopedic Dictionary of Polymers, 899. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_13953.

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Vey, Alain. "Humoral Encapsulation". W Insect Immunity, 59–67. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-1618-3_5.

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Kaaya, Godwin P. "Inducible Humoral Antibacterial Immunity in Insects". W Insect Immunity, 69–89. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-1618-3_6.

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Nauta, Jozef. "Humoral and Cellular Immunity". W Springer Series in Pharmaceutical Statistics, 15–19. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-37693-2_2.

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Williams, Ralph C. "Regulation of Humoral Immunity". W Principles of Molecular Medicine, 251–58. Totowa, NJ: Humana Press, 1998. http://dx.doi.org/10.1007/978-1-59259-726-0_28.

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Smirnova, Olga A. "Radiation and Humoral Immunity". W Environmental Radiation Effects on Mammals, 121–49. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-7213-2_4.

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Streszczenia konferencji na temat "Humoral immunity"

Tian, Yuling, i Peng Ren. "A Clustering Model Inspired by Humoral Immunity". W 2009 International Workshop on Intelligent Systems and Applications. IEEE, 2009. http://dx.doi.org/10.1109/iwisa.2009.5072611.

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Michel, Kristin. "The regulation of humoral control immunity in mosquitoes". W 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.92697.

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Badamshina, G. G., E. P. Sizova i L. M. Fatkhutdinova. "STUDY OF HUMORAL IMMUNITY TO INFECTIONS IN MEDICAL WORKERS". W The 16th «OCCUPATION and HEALTH» Russian National Congress with International Participation (OHRNC-2021). FSBSI “IRIOH”, 2021. http://dx.doi.org/10.31089/978-5-6042929-2-1-2021-1-44-47.

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Abstract: Introduction. In the course of their work, medical workers are exposed to a biological factor, including bacterial, viral nature. Medical personnel come into contact with patients with measles, rubella, diphtheria, tuberculosis, hepatitis, coronavirus infection and other infectious diseases. The aim of the study is to assess the humoral immunity by the presence antibodies to the measles, rubella, hepatitis B viruses, to the causative agent COVID-19, tuberculosis and diphtheria bacteria in health care workers. Methods. Antibodies to measles, rubella, hepatitis B viruses, diphtheria and tetanus pathogens were measured in blood serum samples of 1221 MW; total antibodies to mycobacterium tuberculosis - in 120 MW; antibodies to the nucleocapsid protein of the SARS-CoV-2 virus – in 301 MW. The study was carried out by the method of enzyme immunoassay using commercial test systems; antibodies to diphtheria toxoid were detected in the passive hemagglutination reaction. The control group consisted of persons of engineering and technical personnel, comparable in age, gender and work experience. Results. Medical personnel were found to have significantly more frequent detection of seronegative reactions to the presence of antibodies to the hepatitis B virus (40.9% and 13.5%, p<0.001) of measles (28.8% and 3.9%, p<0.05); significantly high prevalence in the presence of total antibodies to mycobacterium tuberculosis (7.5% of cases in medical, 0% of cases of workers in the control group, p<0.05). In comparison with doctors, nurses had a significantly higher prevalence of antibodies to the nucleocapsid of the SARS-CoV-2 virus (38.9% and 23.7%, p<0.05). Conclusions. The study of post-vaccination immunity in medical workers showed the presence of a high proportion of seronegative individuals among vaccinated (viral hepatitis B, measles) medical workers and, accordingly, significant biological risks. A higher seroprevalence in total antibodies to Mycobacterium tuberculosis may also indicate insufficient immune protection among MW. The biological significance of seroprevalence to SARS-CoV-2 virus proteins (for nurses) requires further study.

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Orlenkovich, Lilija. "CORRELATIONS ANALYSIS OF IMMUNE SYSTEM AND GUT MICROBIOTA INDICES OF RATS IN THE CHRONIC EXPOSITION TO BIOINSECTICIDE ENTOMOPHTHORIN". W XIV International Scientific Conference "System Analysis in Medicine". Far Eastern Scientific Center of Physiology and Pathology of Respiration, 2020. http://dx.doi.org/10.12737/conferencearticle_5fd728a1ea3837.21988844.

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The analysis of the variation in the number, intensity and direction of correlations between the immune system and the gut microbiota of rats revealed that the T-, B-system and humoral immunity changes as well as cellular and humoral factors of an organism nonspecific defense are accompanied by changes of the Intestinal microbiota of intact and experimental rats

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Tyumonbaeva, N. B., A. A. Kazybekova, N. J. Mamytova i A. J. Myrzakulova. "Peculiarities of immunophysiological shifts in adaptation to climatic and geographical conditions of mountains". W 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.

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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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Huba, Y. V., O. V. Myronenko, O. V. Plekhanova i H. A. Garagulya. "Is it really so important to study humoral immunity to SARS-CoV-2?" W ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.1733.

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Pylayeva-Gupta, Yuliya, i Bhalchandra Mirlekar. "Abstract PR06: Reprogramming of naïve B cells in pancreatic cancer subverts humoral immunity". W Abstracts: AACR Virtual Special Conference: Tumor Immunology and Immunotherapy; October 5-6, 2021. American Association for Cancer Research, 2022. http://dx.doi.org/10.1158/2326-6074.tumimm21-pr06.

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Hasanova, Albina, Mikhail Kostinov, Irina Solov’ Ova, Olga Kalinovskaya, Pradeep Baghel i Maksim Abdulkin. "The effect of interferon-alpha-2b therapy on humoral immunity after COVID-19 infection". W ERS Lung Science Conference 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/23120541.lsc-2022.223.

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Zborovsky, AB, IP Gontar, AV Alexandrov, LA Maslakova, GF Sychova i OI Emelyanova. "AB0105 Dynamics of humoral immunity indices in systemic sclerosis patients depending on the therapy carried out". W Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.253.

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Pradeep, B. G. Sampath Aruna, i Hazrat Ali. "Global stability properties for a delayed virus dynamics model with humoral immunity response and absorption effect". W 2017 International Conference on Electrical Engineering (ICEE). IEEE, 2017. http://dx.doi.org/10.1109/icee.2017.7893424.

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Raporty organizacyjne na temat "Humoral immunity"

Rusanova, O. A., I. P. Gontar, O. A. Emelyanova, L. A. Maslakova i Yi A. Trubenko. MANIFESTATIONS OF HUMORAL IMMUNITY TO FIBRONECTIN AS PART OF CLINICAL PRESENTATIONS OF RHEUMATOID ARTHRITIS. Планета, 2018. http://dx.doi.org/10.18411/978-5-907109-24-7-2018-xxxiv-97-99.

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Middlebrooks, Bobby L. Investigation of the Role of Immunoglobulin Classes and Subclasses in Humoral and Mucosal Immunity in Cetaceans. Fort Belvoir, VA: Defense Technical Information Center, czerwiec 2005. http://dx.doi.org/10.21236/ada452454.

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Gontar, I. P., O. A. Rusanova, A. S. Trofimenko, O. I. Emelyanova, L. A. Maslakova i N. Emelyanov. CARDIOVASCULAR CONDITIONS IN PATIENTS WITH SYSTEMIC SCLERODERMA THAT ARE ASSOCIATED WITH HUMORAL IMMUNITY IMPAIRMENT TO ELASTIN AND ELSTASE. Планета, 2018. http://dx.doi.org/10.18411/978-5-907109-24-7-2018-xxxiv-54-55.

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Chejanovsky, Nor, i Bruce A. Webb. Potentiation of pest control by insect immunosuppression. United States Department of Agriculture, lipiec 2004. http://dx.doi.org/10.32747/2004.7587236.bard.

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Our original aims were to elucidate the mechanisms through which the immunosuppressive insect virus, the Campoletis sonorensis polydnavirus (CsV) promotes replication of a well-characterized pathogenic virus, the Autographa californica multiple nucleopolyhedrovirus (AcMNPV) in hosts that are mildly or non-permissive to virus replication. According to the BARD panels criticism we modified our short-term goals (see below). Thus, in this feasibility study (one-year funding) we aimed to show that: 1. S. littoralis larvae mount an immune response against a baculovirus infection. 2. Immunosuppression of an insect pest improves the ability of a viral pathogen (a baculovirus) to infect the pest. 3. S. littoralis cells constitute an efficient tool to study some aspects of the anti- viral immune response. We achieved the above objectives by: 1. Finding melanized viral foci upon following the baculoviral infection in S . littoralis larvae infected with a polyhedra - positive AcMNPV recombinant that expressed the GFP gene under the control of the Drosophila heat shock promoter. 2. Studying the effect of AcMNPV-infection in S . littoralis immunosuppressed by parasitation with the Braconidae wasp Chelonus inanitus that bears the CiV polydna virus, that resulted in higher susceptibility of S. littoralis to AcMNPV- infection. 3. Proving that S. littoralis hemocytes resist AcMNPV -infection. 4. Defining SL2 as a granulocyte-like cell line and demonstrating that as littoralis hemocytic cell line undergoes apoptosis upon AcMNPV -infection. 5. Showing that some of the recombinant AcMNPV expressing the immuno-suppressive polydna virus CsV- vankyrin genes inhibit baculoviral-induced lysis of SL2 cells. This information paves the way to elucidate the mechanisms through which the immuno- suppressive polydna insect viruses promote replication of pathogenic baculoviruses in lepidopteran hosts that are mildly or non-permissive to virus- replication by: - Assessing the extent to which and the mechanisms whereby the immunosuppressive viruses, CiV and CsV or their genes enhance AcMNPV replication in polydnavirus- immunosuppressed H. zea and S. littoralis insects and S. littoralis cells. - Identifying CiV and CsV genes involved in the above immunosuppression (e.g. inhibiting cellular encapsulation and disrupting humoral immunity). This study will provide insight to the molecular mechanisms of viral pathogenesis and improve our understanding of insect immunity. This knowledge is of fundamental importance to controlling insect vectored diseases of humans, animals and plants and essential to developing novel means for pest control (including baculoviruses) that strategically weaken insect defenses to improve pathogen (i.e. biocontrol agent) infection and virulence.

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

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

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Gershoni, Jonathan M., David E. Swayne, Tal Pupko, Shimon Perk, Alexander Panshin, Avishai Lublin i Natalia Golander. Discovery and reconstitution of cross-reactive vaccine targets for H5 and H9 avian influenza. United States Department of Agriculture, styczeń 2015. http://dx.doi.org/10.32747/2015.7699854.bard.

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Research objectives: Identification of highly conserved B-cell epitopes common to either H5 or H9 subtypes of AI Reconstruction of conserved epitopes from (1) as recombinantimmunogens, and testing their suitability to be used as universal vaccine components by measuring their binding to Influenza vaccinated sera of birds Vaccination of chickens with reconstituted epitopes and evaluation of successful vaccination, clinical protection and viral replication Development of a platform to investigate the dynamics of immune response towards infection or an epitope based vaccine Estimate our ability to focus the immune response towards an epitope-based vaccine using the tool we have developed in (D) Summary: This study is a multi-disciplinary study of four-way collaboration; The SERPL, USDA, Kimron-Israel, and two groups at TAU with the purpose of evaluating the production and implementation of epitope based vaccines against avian influenza (AI). Systematic analysis of the influenza viral spike led to the production of a highly conserved epitope situated at the hinge of the HA antigen designated “cluster 300” (c300). This epitope consists of a total of 31 residues and was initially expressed as a fusion protein of the Protein 8 major protein of the bacteriophagefd. Two versions of the c300 were produced to correspond to the H5 and H9 antigens respectively as well as scrambled versions that were identical with regard to amino acid composition yet with varied linear sequence (these served as negative controls). The recombinantimmunogens were produced first as phage fusions and then subsequently as fusions with maltose binding protein (MBP) or glutathioneS-transferase (GST). The latter were used to immunize and boost chickens at SERPL and Kimron. Furthermore, vaccinated and control chickens were challenged with concordant influenza strains at Kimron and SEPRL. Polyclonal sera were obtained for further analyses at TAU and computational bioinformatics analyses in collaboration with Prof. Pupko. Moreover, the degree of protection afforded by the vaccination was determined. Unfortunately, no protection could be demonstrated. In parallel to the main theme of the study, the TAU team (Gershoni and Pupko) designed and developed a novel methodology for the systematic analysis of the antibody composition of polyclonal sera (Deep Panning) which is essential for the analyses of the humoral response towards vaccination and challenge. Deep Panning is currently being used to monitor the polyclonal sera derived from the vaccination studies conducted at the SEPRL and Kimron.

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