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Artykuły w czasopismach na temat "Vaccination – Genetic aspects"
Bondarev, V. P., V. A. Shevtsov, I. N. Indikova, E. E. Evreinova i D. V. Gorenkov. "Rotavirus Epidemiology and Vaccination Tactics". BIOpreparations. Prevention, Diagnosis, Treatment 19, nr 2 (16.06.2019): 81–87. http://dx.doi.org/10.30895/2221-996x-2019-19-2-81-87.
Pełny tekst źródłaPIKUŁA, ANNA, i KRZYSZTOF ŚMIETANKA. "Selected aspects of infectious bursal disease – the current state of knowledge". Medycyna Weterynaryjna 74, nr 10 (2023): 6138–2023. http://dx.doi.org/10.21521/mw.6138.
Pełny tekst źródłaTeale, Alan. "Biotechnology: a key element in the CGIAR's livestock research programme". Outlook on Agriculture 26, nr 4 (grudzień 1997): 217–25. http://dx.doi.org/10.1177/003072709702600403.
Pełny tekst źródłaHELGESSON, GERT, i STEFAN ERIKSSON. "Four Themes in Recent Swedish Bioethics Debates". Cambridge Quarterly of Healthcare Ethics 20, nr 3 (20.05.2011): 409–17. http://dx.doi.org/10.1017/s0963180111000090.
Pełny tekst źródłaMehra, Narinder K., i Gurvinder Kaur. "MHC-based vaccination approaches: progress and perspectives". Expert Reviews in Molecular Medicine 5, nr 7 (24.02.2003): 1–17. http://dx.doi.org/10.1017/s1462399403005957.
Pełny tekst źródłaTusup, Marina, Lars E. French, Mara De Matos, David Gatfield, Thomas Kundig i Steve Pascolo. "Design of in vitro Transcribed mRNA Vectors for Research and Therapy". CHIMIA International Journal for Chemistry 73, nr 5 (29.05.2019): 391–94. http://dx.doi.org/10.2533/chimia.2019.391.
Pełny tekst źródłaAmbinder, Alexander J., Pareen J. Shenoy, Neha Malik, Alison Maggioncalda, Loretta J. Nastoupil i Christopher R. Flowers. "Exploring Risk Factors for Follicular Lymphoma". Advances in Hematology 2012 (2012): 1–13. http://dx.doi.org/10.1155/2012/626035.
Pełny tekst źródłaEckmann, Lars, i Frances D. Gillin. "Microbes and Microbial Toxins: Paradigms for Microbial- Mucosal Interactions I. Pathophysiological aspects of enteric infections with the lumen-dwelling protozoan pathogenGiardia lamblia". American Journal of Physiology-Gastrointestinal and Liver Physiology 280, nr 1 (1.01.2001): G1—G6. http://dx.doi.org/10.1152/ajpgi.2001.280.1.g1.
Pełny tekst źródłaEckert, Johannes, i Peter Deplazes. "Biological, Epidemiological, and Clinical Aspects of Echinococcosis, a Zoonosis of Increasing Concern". Clinical Microbiology Reviews 17, nr 1 (styczeń 2004): 107–35. http://dx.doi.org/10.1128/cmr.17.1.107-135.2004.
Pełny tekst źródłaSang, Helen. "DISEASE RESISTANCE AND OTHER APPLICATIONS OF TRANSGENESIS IN THE CHICKEN". Reproduction, Fertility and Development 25, nr 1 (2013): 320. http://dx.doi.org/10.1071/rdv25n1ab345.
Pełny tekst źródłaRozprawy doktorskie na temat "Vaccination – Genetic aspects"
Baynam, Gareth. "Genetic influences on vaccine response in children". University of Western Australia. School of Paediatrics and Child Health, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0259.
Pełny tekst źródłaHollister, Kristin N. "Elucidating the role of BCL6 in helper T cell activation, proliferation, and differentiation". Thesis, 2014. http://hdl.handle.net/1805/5930.
Pełny tekst źródłaThe transcriptional repressor BCL6 has been shown to be essential for the differentiation of germinal center (GC) B cells and follicular T helper (TFH) cells. The interaction of TFH and GC B cells is necessary for the development of high affinity antibodies specific for an invading pathogen. Germline BCL6-deficient mouse models limit our ability to study BCL6 function in T cells due to the strong inflammatory responses seen in these mice. To overcome this, our lab has developed a new BCL6 conditional knockout (cKO) mouse using the cre/lox system, wherein the zinc finger region of the BCL6 gene is flanked by loxP sites. Mating to a CD4-Cre mouse allowed us to study the effects of BCL6 loss specifically in T cells, without the confounding effects seen in germline knockout models. Using this cKO model, we have reaffirmed the necessity of BCL6 for TFH differentiation, including its role in sustained CXCR5 surface expression, a signature marker for TFH cells. This model also allowed us to recognize the role of BCL6 in promoting the expression of PD-1, another key surface marker for TFH cells. Without BCL6, CD4+ T cells cannot express PD-1 at the high levels seen on TFH cells. Our discovery of DNMT3b as a target for BCL6 suggests BCL6-deficient T cells have increased DNA methyltransferase activity at the PD-1 promoter. This data establishes a novel pathway for explaining how BCL6, a transcriptional repressor, can activate genes. Experiments with the BCL6 cKO model have also established a role for BCL6 in naïve CD4+ T cell activation. Furthermore, we did not observe increased differentiation of other helper T cell subsets, in contrast to what has been reported elsewhere with germline BCL6-deficient models. Unexpectedly, we found decreased T helper type 2 (Th2) cells, whereas mouse models with a germline mutation of BCL6 have increased Th2 cells. These results indicate that BCL6 activity in non-T cells is critical for controlling T cell differentiation. Finally, using an HIV-1 gp120 immunization model, we have, for the first time, shown BCL6-dependent GCs to be limiting for antibody development and affinity maturation in a prime-boost vaccine scheme.
Książki na temat "Vaccination – Genetic aspects"
Kampourakis, Kostas, i Kevin McCain. Uncertainty. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780190871666.001.0001.
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