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Relevant bibliographies by topics / Experimental Autoimmune Encephalomyelitis, Progesterone / Dissertations / Theses

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Dissertations / Theses on the topic 'Experimental Autoimmune Encephalomyelitis, Progesterone'

Author: Grafiati

Published: 9 March 2023

Last updated: 31 July 2025

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1

BALLARINI, ELISA. "Caratterizzazione di un modello di encefalomielite autoimmune sperimentale e ruolo neuroprotettivo del progesterone." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2012. http://hdl.handle.net/10281/39833.

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Studies concerning the role of neuroactive steroids in chronic models of Experimental Autoimmune Encephalomyelitis (EAE) are still scarce. First we considered different pathological targets in Dark Agouti (DA) rats affected by EAE in order to well characterize this chronic model of Multiple Sclerosis (MS) which well reflects the relapsing-remitting form of MS. We analyzed neuroinflammatory profile, assonopathy and neuroactive steroid levels in the spinal cord of DA rats affected by EAE. Data obtained at 14 dpi (i.e. days post induction) showed that acute neurological signs were associated wi

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2

Harness, Jacqueline. "Immunoregulation of experimental autoimmune encephalomyelitis /." St. Lucia, Qld, 2002. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe17375.pdf.

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3

Isaksson, Magnus. "Initiation of Autoimmunity in Experimental Autoimmune Encephalomyelitis." Doctoral thesis, Uppsala universitet, Molekylär medicin, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-173427.

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The events that trigger an autoimmune disease remain largely unknown. To study these events animal models are necessary because symptoms of autoimmune diseases are preceded by a long asymptomatic period in humans. Experimental autoimmune encephalomyelitis (EAE) is the best characterized model for cell mediated autoimmunity and an animal model for the human disease multiple sclerosis. EAE is induced in rodents by immunization with myelin antigens (Ags) together with adjuvants. After immunization, T cells are primed in the periphery by Ag presenting cells and subsequently invade the central nerv

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4

Ruppova, Klara. "Role of eosinophils in experimental autoimmune encephalomyelitis." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2017. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-231835.

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Experimental autoimmune encephalomyelitis (EAE) is the rodent model of multiple sclerosis (MS), a chronic autoimmune neuroinflammatory disease that has a devastating impact on various neurological functions of the patients. The hallmarks of both, MS and EAE, are neuroinflammation, demyelination and neuroaxonal degeneration. Various types of lymphoid and myeloid cells were shown to infiltrate the central nervous system and to participate in disease pathology. However, the role of eosinophil granulocytes has been less explored thus far. An early study showed that eosinophils infiltrate into the

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5

Weissert, Robert. "Immunogenetics and treatment of experimental autoimmune encephalomyelitis /." Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3645-5/.

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6

Lobell, Anna. "Suppressive DNA vaccination in experimental autoimmune encephalomyelitis /." Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3782-6/.

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7

Dowdell, Kennichi C. "Neuroendocrine regulation of relapsing Experimental Autoimmune Encephalomyelitis /." The Ohio State University, 1999. http://rave.ohiolink.edu/etdc/view?acc_num=osu1488191124569455.

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8

Wefer, Judit. "Studies of cellular pathogenesis in experimental autoimmune encephalomyelitis /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7140-023-0/.

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9

Wållberg, Maja. "Modulation of immune responses in experimental autoimmune encephalomyelitis /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-335-3/.

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10

Berl, Sabina [Verfasser]. "Neuronal Response to Experimental Autoimmune Encephalomyelitis / Sabina Berl." Mainz : Universitätsbibliothek Mainz, 2020. http://d-nb.info/1203322933/34.

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11

Koutrolos, Michail. "Role of regulatory T cells in experimental autoimmune encephalomyelitis." Diss., Ludwig-Maximilians-Universität München, 2013. http://nbn-resolving.de/urn:nbn:de:bvb:19-161896.

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12

Tran, Elise H. "Immune invasion and glial activation in experimental autoimmune encephalomyelitis." Thesis, McGill University, 2000. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=36845.

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Leukocyte recruitment into tissues in response to infection or injury is a crucial event for the elimination of pathogens to protect the host. However, when leukocytes invade the central nervous system (CNS) and neuromflammatory disorders result, neurological function may be compromised. Infiltration of the CNS, predominantly by T cells and macrophages, characterizes Multiple Sclerosis and its animal counterpart, Experimental Autoimmune Encephalomyelitis (EAE).<br>Autoreactive T cells that initiate EAE produce Th1 cytokines (e.g., IFNgamma, TNFalpha). Nevertheless, previous studies also indica

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13

Fuller, Kathleen Ann. "Oral tolerance in experimental autoimmune encephalomyelitis : the humoral arm /." The Ohio State University, 1990. http://rave.ohiolink.edu/etdc/view?acc_num=osu148767684711592.

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14

Jagodić, Maja. "The complex genetics of experimental autoimmune neuroinflammation /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7140-157-1/.

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15

DE, CEGLIA ROBERTA. "Unraveling the role of cns acidosis in experimental autoimmune encephalomyelitis." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2013. http://hdl.handle.net/10281/46925.

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Multiple Sclerosis (MS) is an inflammatory demyelinating disease of the Central Nervous System (CNS) featuring severe neuronal degenerative processes. Emerging findings indicate that several injurious molecular and cellular cascades are contributing to neurodegeneration. Among them, CNS acidosis has been recently demonstrated to have a detrimental role in Experimental Autoimmune Encephalomyelitis (EAE). Good candidates to trigger acidosis-mediated neurodegeneration are represented by Acid Sensing Ion Channels (ASICs) which are H+-gated cation channels of the CNS. We measured CNS acidosis in EA

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16

Eltayeb, Sana. "Chemokine receptor expression and function in experimental autoimmune neuroimflammation /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-197-5/.

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17

Duan, Rui-Sheng. "Inflammation and neurodegeneration in mouse nervous system: experimental application /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-606-9/.

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18

Papenfuss, Tracey L. "Hormones and dendritic cells influences on the initiation of the autoimmune disease experimental autoimmune encephalomyelitis /." Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1173196704.

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19

Kalyvas, Athena. "The role of the phospholipase A₂ family in experimental autoimmune encephalomyelitis /." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111895.

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Multiple Sclerosis (MS) is an autoimmune disease of the central nervous system (CNS) that is characterized by widespread focal areas of inflammation and demyelination. Although the exact cause of the disease is still not known, myelin-reactive T cells that enter the CNS trigger the disease and lead to the recruitment and activation of macrophages and other immune cells. One set of candidates that could serve to mediate these CNS changes is the family of phospholipase A2 (PLA2) enzymes, which consist of secreted (sPLA2) and cytosolic (cPLA2) forms. These enzymes hydrolyze membrane phospholipids

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20

Anwar, Mohammad Ashraful. "SPARC modulates the spinal cord neuroimmune response in experimental autoimmune encephalomyelitis." Thesis, University of British Columbia, 2014. http://hdl.handle.net/2429/46047.

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SPARC (Secreted Protein Acidic and Rich in Cysteine), a secreted glycoprotein, regulates proliferation, migration and differentiation. SPARC is highly expressed in glia and blood vessels during CNS development. SPARC expression is maintained in tissues undergoing rapid turnover and its expression is highly upregulated during injury or disease. SPARC’s modulatory activity in glia and endothelia during injury lead us to investigate the role of SPARC in an animal model of CNS inflammation and demyelination with known BBB dysfunction: Experimental Autoimmune Encephalomyelitis (EAE). We discovered

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21

Srinivasan, Mythily. "Costimulatory blockade by CD28 Peptide mimics : suppression of experimental Autoimmune Encephalomyelitis /." The Ohio State University, 2001. http://rave.ohiolink.edu/etdc/view?acc_num=osu1488205318509738.

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22

Esaki, Yoshiyasu. "Dual roles of PGE2-EP4 signaling in mouse experimental autoimmune encephalomyelitis." Kyoto University, 2011. http://hdl.handle.net/2433/142551.

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23

MARCONI, Silvia. "Therapeutic efficacy of adipose-derived MSC in chronic experimental autoimmune encephalomyelitis." Doctoral thesis, Università degli Studi di Verona, 2010. http://hdl.handle.net/11562/343596.

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Le cellule staminali mesenchimali (CSM) rappresentano un promettente approccio terapeutico per le patologie neurologiche a carattere autoimmune. In lavori precedenti è stato dimostrato che il trattamento con CSM da midollo osseo in un modello di encefalite autoimmune sperimentale (EAS), modello animale di sclerosi multipla, ha un effetto immunomodulate ed è in grado di ridurre la gravità della malattia. In questo lavori dimostriamo che la somministrazione di CSM da tessuto adiposo (CSA) prima dell'insorgenza della malattia è in grado di ridurre significativamente la gravità della malattia, di

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24

PETROSINO, VALENTINA. "MOLECULAR MECHANISMS UNDELYING REST DYSREGULATION IN THE EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS (EAE)." Doctoral thesis, Università degli studi di Genova, 2019. http://hdl.handle.net/11567/945765.

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The development and maturation of the nervous system imply a precise temporal and spatial modulation of gene expression, coordinated by transcriptional enhancers and repressors. In this context, the key role of repressor element 1-silencing transcription factor (REST) is largely known. REST regulates neurogenesis and neuronal identity through cell-specific gene repression, allowing expression of its targets in mature neurons. During neuronal development REST levels are reduced and REST is quiescent in mature neurons, which are able to modulate its expression in response to pathological stimuli

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25

Axtell, Robert C. "The role of CD5 in experimental autoimmune encephalitomyelitis." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2007. http://www.mhsl.uab.edu/dt/2007p/axtell.pdf.

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26

de, Graaf Katrien L. "Molecular basis for the MHC class II association in rat experimental autoimmune encephalomyelitis /." Stockholm, 2001. http://diss.kib.ki.se/2001/91-628-4857-7/.

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27

Short, Abigail E. "The role of MIF production by B lymphocytes in experimental autoimmune encephalomyelitis." Connect to resource, 2010. http://hdl.handle.net/1811/45462.

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28

Esposito, Marianna. "Immune Regulation in Experimental Autoimmune Encephalomyelitis : the Role of Regulatory T cells." Thesis, Open University, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.503627.

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29

Agnello, Davide. "Erythropoietin crosses the blood-brain barrier and protects against experimental autoimmune encephalomyelitis." Dijon, 2003. http://www.theses.fr/2003DIJOMU05.

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L'érythropoi͏̈étine (EPO), administrée par voie systémique, traverse la barrière hématoméningée et a chez l'animal des effets protecteurs sur l'ischémie cérébrale, le traumatisme cérébral et protège également de l'encéphalomyélite autoimmune expérimentale chez le rat. Dans un second travail, nous avons caractérisé l'effet de l'administration systémique d'EPO sur la composante inflammatoire induite lors de l'encéphalopathie autoimmune expérimentale aigue͏̈ chez le rat Lewis. L'administration quotidienne d'EPO aux doses de 500-500 U/kg en intrapéritonéal à partir du 3e jour après l'immunisation

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30

Azzam, Sausan. "Protein Profiling Analysis of Multiple Sclerosis and Experimental Autoimmune Encephalomyelitis Brain Tissue." Kent State University / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=kent1302472724.

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31

Yang, Jinghui. "Peripheral immune response in chronic relapsing experimental autoimmune encephalomyelitis in SJL mice." Helsinki : University of Helsinki, 2003. http://ethesis.helsinki.fi/julkaisut/laa/haart/vk/yang/.

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32

WOLDETSADIK, ABIY DEMEKE. "Development of nanoparticle platforms for “inverse vaccination” in experimental autoimmune encephalomyelitis (EAE)." Doctoral thesis, Università del Piemonte Orientale, 2014. http://hdl.handle.net/11579/46149.

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33

Xu, Ling-Yun. "Mechanisms and modulation of experimental allergic encephalomyelitis as basis for treatment of multiple sclerosis /." Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4452-0/.

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34

Lassmann, Silke. "Antigen-dependent regulation of cytokine and chemokine expression in EAE." Thesis, University of London, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.287992.

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35

Dahlman, Ingrid. "Genetic dissection of experimental autoimmune neuroinflammatory diseases in rats /." Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3768-0/.

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36

Vuong, Linda. "Toll-like receptor 7 tolerance in anti-neuroinflammation in murine experimental autoimmune encephalomyelitis." Diss., [La Jolla] : University of California, San Diego, 2010. http://wwwlib.umi.com/cr/fullcit?p1477944.

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Thesis (M.S.)--University of California, San Diego, 2010.<br>Title from first page of PDF file (viewed July 12, 2010). Available via ProQuest Digital Dissertations. Includes bibliographical references (leaves 50-64).

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37

Jabs, Claudia. "Roles of the B7-CD28 superfamily in the regulation of experimental autoimmune encephalomyelitis." [S.l.] : [s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=964802090.

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38

Abdul-Majid, Khairul-Bariah. "Pathogenesis of myelin oligodendrocyte glycoprotein induced experimental autoimmune encephalomyelitis in DBA/1 mice /." Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-112-8/.

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39

Floßdorf, Juliane [Verfasser]. "The role of PPARγ in myeloid cells in experimental autoimmune encephalomyelitis / Juliane Floßdorf". Bonn : Universitäts- und Landesbibliothek Bonn, 2013. http://d-nb.info/1044970332/34.

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40

Meyer, Abbie L. "Oral tolerance to myelin basic protein in mice : suppression of experimental autoimmune encephalomyelitis /." The Ohio State University, 1996. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487934589975749.

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41

Wohler, Jillian E. "The role of the [beta]₂-integrin family on T cell subsets." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2009. https://www.mhsl.uab.edu/dt/2009p/wohler.pdf.

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42

Steinbach, Karin [Verfasser], and Roland [Akademischer Betreuer] Martin. "Role of autoimmune inflammation and impaired neurodegeneration in the pathogenesis of experimental autoimmune encephalomyelitis / Karin Steinbach. Betreuer: Roland Martin." Hamburg : Staats- und Universitätsbibliothek Hamburg, 2011. http://d-nb.info/1020384395/34.

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43

McClain, Melanie A. "Pregnancy and the post-partum period regulate experimental autoimmune encephalomyelitis through immunoregulatory cytokine production." Connect to this title online, 2005. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1119898792.

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Thesis (Ph. D.)--Ohio State University, 2005.<br>Title from first page of PDF file. Document formatted into pages; contains xv, 95 p.; also includes graphics (some col.) Includes bibliographical references (p. 85-95). Available online via OhioLINK's ETD Center

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44

Schubart, Anna. "Aspects of the Immunobiology of Myelin Oligodendrocyte Glycoprotein (MOG)-induced Experimental Autoimmune Encephalomyelitis (EAE)." Diss., lmu, 2002. http://nbn-resolving.de/urn:nbn:de:bvb:19-1011.

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45

Mohammadi, Mahvelati Tara. "The Nod-like receptor, Nlrp12, plays an anti-inflammatory role in experimental autoimmune encephalomyelitis." Mémoire, Université de Sherbrooke, 2017. http://hdl.handle.net/11143/11612.

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Abstract : Multiple Sclerosis (MS) is an organ-specific autoimmune disease characterized by the presence of demyelinating plaques throughout the central nervous system (CNS) as a result of an abnormal inflammatory response. During MS, activated microglia can play the role of antigen presenting cells and can, therefore, skew T cell responses towards a pro-inflammatory phenotype. Once activated, microglia upregulate the expression of pro-inflammatory molecules. In addition to microglial responses during MS, astrocytes are also implicated in the development of MS lesions. Upon injury and nearby n

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46

Sim, Deborah. "Dynamic Intravital Imaging of Immune Cells During the Initiating Events of Experimental Autoimmune Encephalomyelitis." Case Western Reserve University School of Graduate Studies / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=case1396560202.

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47

Griffin, Ann Christine. "The influences of gender and neuroendocrine reactivity in the modulation of experimental autoimmune encephalomyelitis /." The Ohio State University, 1992. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487778663284975.

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48

Wu, Xingchen. "Multiple sclerosis : MRI diagnosis, potential treatment and future potential for nanoparticle applications /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-515-1/.

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49

Martínez, Membrives Esther. "Susceptibility to experimental autoimmune encephalomyelitis (model of multiple sclerosis) and anxiety in genetically heterogeneous rats." Doctoral thesis, Universitat Autònoma de Barcelona, 2012. http://hdl.handle.net/10803/123299.

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Las respuestas al estrés del eje hipotalámico-pituitario-adrenal (HPA) juegan un papel decisivo tanto en la conducta ansiosa como en el funcionamiento del sistema inmune (IS). Es sabido que los niveles elevados de glucocorticoides (GC) desempeñan un papel protector ante la encefalomielitis experimental autoinmune (EAE), fiable modelo animal de la esclerosis múltiple. En esta Tesis, nos propusimos investigar si un determinado perfil ansioso podría corresponderse con un perfil específico de sensibilidad a la inflamación. En el “Estudio I”, ratas genéticamente heterogéneas N/Nih-HS de ambos sex

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50

Berard, Jennifer. "Immune mediators involved in the differential pathogenesis of relapsing-remitting and chronic experimental autoimmune encephalomyelitis." Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=92223.

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Multiple sclerosis (MS) is a disease of the central nervous system (CNS) that is characterized by inflammation, demyelination, and axonal loss. These characteristic histopathological features of MS are similar to those seen in the animal model experimental autoimmune encephalomyelitis (EAE), a T cell-mediated demyelinating disease. Importantly, many of the immune mediators involved in EAE pathogenesis have also been implicated in MS. Like MS, EAE is a heterogeneous disease that can follow either a relapsing-remitting or a chronic disease course. However, the molecular and pathogenic differ

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