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Journal articles on the topic "Sclerosi multipla peptides"
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Bourdette, D. N., E. Edmonds, C. Smith, J. D. Bowen, C. RG Guttmann, Z. P. Nagy, J. Simon, et al. "A highly immunogenic trivalent T cell receptor peptide vaccine for multiple sclerosis." Multiple Sclerosis Journal 11, no. 5 (October 2005): 552–61. http://dx.doi.org/10.1191/1352458505ms1225oa.
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Background: T cell receptor (TCR) peptide vaccination is a novel approach to treating multiple sclerosis (MS). The low immunogenicity of previous vaccines has hindered the development of TCR peptide vaccination for MS. Objective: To compare the immunogenicity of intramuscular injections of TCR BV5S2, BV6S5 and BV13S1 CDR2 peptides in incomplete Freund’s adjuvant (IFA) with intradermal injections of the same peptides without IFA. Methods: MS subjects were randomized to receive TCR peptides/IFA, TCR peptides/saline or IFA alone. Subjects were on study for 24 weeks. Results: The TCR peptides/IFA vaccine induced vigorous T cell responses in 100% of subjects completing the 24-week study (9/9) compared with only 20% (2/10) of those receiving the TCR peptides/saline vaccine (P =0.001). IFA alone induced a weak response in only one of five subjects. Aside from injection site reactions, there were no significant adverse events attributable to the treatment. Conclusions: The trivalent TCR peptide in IFA vaccine represents a significant improvement in immunogenicity over previous TCR peptide vaccines and warrants investigation of its ability to treat MS.
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Matsoukas, John, George Deraos, Kostas Kelaidonis, Md Kamal Hossain, Jack Feehan, Andreas G. Tzakos, Elizabeth Matsoukas, Emmanuel Topoglidis, and Vasso Apostolopoulos. "Myelin Peptide–Mannan Conjugate Multiple Sclerosis Vaccines: Conjugation Efficacy and Stability of Vaccine Ingredient." Vaccines 9, no. 12 (December 8, 2021): 1456. http://dx.doi.org/10.3390/vaccines9121456.
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Myelin peptide–mannan conjugates have been shown to be potential vaccines in the immunotherapy of multiple sclerosis. The conjugates are comprised from the epitope peptide and the polysaccharide mannan which transfers as a carrier the antigenic peptide to dendritic cells that process and present antigenic peptides at their surface in complex with MHC class I or class II resulting in T-cell stimulation. The conjugation of antigenic peptide with mannan occurs through the linker (Lys–Gly)5, which connects the peptide with the oxidized mannose units of mannan. This study describes novel methods for the quantification of the vaccine ingredient peptide within the conjugate, a prerequisite for approval of clinical trials in the pursuit of multiple sclerosis therapeutics. Myelin peptides, such as MOG35–55, MBP83–99, and PLP131–145 in linear or cyclic form, as altered peptide ligands or conjugated to appropriate carriers, possess immunomodulatory properties in experimental models and are potential candidates for clinical trials.
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Bourdette, D. N., R. H. Whitham, Y. K. Chou, W. J. Morrison, J. Atherton, C. Kenny, D. Liefeld, G. A. Hashim, H. Offner, and A. A. Vandenbark. "Immunity to TCR peptides in multiple sclerosis. I. Successful immunization of patients with synthetic V beta 5.2 and V beta 6.1 CDR2 peptides." Journal of Immunology 152, no. 5 (March 1, 1994): 2510–19. http://dx.doi.org/10.4049/jimmunol.152.5.2510.
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Abstract Immunization with disease-associated TCR V region peptides is an effective treatment for experimental autoimmune encephalomyelitis. Myelin basic protein-specific T cells, which induce experimental autoimmune encephalomyelitis in many animal strains, may be important in the pathogenesis of multiple sclerosis. Myelin basic protein-specific T cell clones from some multiple sclerosis patients preferentially use TCR V genes from the V beta 5.2 and V beta 6.1 families. To assess the safety and immunogenicity of TCR V beta 5.2 and V beta 6.1 peptides, we injected 11 multiple sclerosis patients with varying doses of two synthetic peptides, TCR V beta 5.2(39-59) and V beta 6.1(39-59), encompassing the CDR2 region of these V gene families. Low doses (100 to 300 micrograms) of peptide induced T cell immunity in 7 of 11 patients to one or both peptides. Delayed type hypersensitivity skin responses to the peptides were observed in three of seven responders, and TCR peptide-specific Ab occurred in two of seven T cell responders. Low doses of TCR peptides produced no side effects and did not cause broad spectrum immunosuppression. Synthetic TCR V region peptides can induce T cell immunity safely in humans and may prove useful in treating human autoimmune diseases.
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Planas, Raquel, Radleigh Santos, Paula Tomas-Ojer, Carolina Cruciani, Andreas Lutterotti, Wolfgang Faigle, Nicole Schaeren-Wiemers, et al. "GDP-l-fucose synthase is a CD4+ T cell–specific autoantigen in DRB3*02:02 patients with multiple sclerosis." Science Translational Medicine 10, no. 462 (October 10, 2018): eaat4301. http://dx.doi.org/10.1126/scitranslmed.aat4301.
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Multiple sclerosis is an immune-mediated autoimmune disease of the central nervous system that develops in genetically susceptible individuals and likely requires environmental triggers. The autoantigens and molecular mimics triggering the autoimmune response in multiple sclerosis remain incompletely understood. By using a brain-infiltrating CD4+ T cell clone that is clonally expanded in multiple sclerosis brain lesions and a systematic approach for the identification of its target antigens, positional scanning peptide libraries in combination with biometrical analysis, we have identified guanosine diphosphate (GDP)–l-fucose synthase as an autoantigen that is recognized by cerebrospinal fluid–infiltrating CD4+ T cells from HLA-DRB3*–positive patients. Significant associations were found between reactivity to GDP-l-fucose synthase peptides and DRB3*02:02 expression, along with reactivity against an immunodominant myelin basic protein peptide. These results, coupled with the cross-recognition of homologous peptides from gut microbiota, suggest a possible role of this antigen as an inducer or driver of pathogenic autoimmune responses in multiple sclerosis.
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Owens, Gregory P., Andrew J. Shearer, Xiaoli Yu, Alanna M. Ritchie, Kathryne M. Keays, Jeffrey L. Bennett, Donald H. Gilden, and Mark P. Burgoon. "Screening Random Peptide Libraries with Subacute Sclerosing PanencephalitisBrain-Derived Recombinant Antibodies Identifies Multiple Epitopes in the C-Terminal Region of the Measles Virus Nucleocapsid Protein." Journal of Virology 80, no. 24 (December 15, 2006): 12121–30. http://dx.doi.org/10.1128/jvi.01704-06.
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ABSTRACT Infectious and inflammatory diseases of the CNS are often characterized by a robust B-cell response that manifests as increased intrathecal immunoglobulin G (IgG) synthesis and the presence of oligoclonal bands. We previously used laser capture microdissection and single-cell PCR to analyze the IgG variable regions of plasma cells from the brain of a patient with subacute sclerosing panencephalitis (SSPE). Five of eight human IgG1 recombinant antibodies (rAbs) derived from SSPE brain plasma cell clones recognized the measles virus (MV) nucleocapsid protein, confirming that the antibody response in SSPE targets primarily the agent causing disease. In this study, as part of our work on antigen identification, we used four rAbs to probe a random phage-displayed peptide library to determine if epitopes within the MV nucleocapsid protein could be identified with SSPE brain rAbs. All four of the SSPE rAbs enriched phage-displayed peptide sequences that reacted specifically to their panning rAb by enzyme-linked immunosorbent assay. BLASTP searches of the NCBI protein database revealed clear homologies in three peptides and different amino acid stretches within the 65 C-terminal amino acids of the MV nucleocapsid protein. The specificities of SSPE rAbs to these regions of the MV nucleocapsid protein were confirmed by binding to synthetic peptides or to short cDNA expression products. These results indicate the feasibility of using peptide screening for antigen discovery in central nervous system inflammatory diseases of unknown etiology, such as multiple sclerosis, neurosarcoidosis, or Behcet's syndrome.
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Beddow, Sara A., Tobias Neef, Igal Ifergan, Joseph R. Podojil, Daniel Getts, and Stephen D. Miller. "Treatment with Multiple-linked Myelin Peptides Encapsulated within Nanoparticles Induces Antigen-specific Tolerance in SJL/J Relapsing-remitting Experimental Autoimmune Encephalomyelitis." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 160.10. http://dx.doi.org/10.4049/jimmunol.204.supp.160.10.
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Abstract Experimental autoimmune encephalomyelitis (EAE) in SJL/J mice is a demyelinating disease of the central nervous system (CNS), and serves as a fit-for-purpose pre-clinical model of Multiple Sclerosis (MS). Data show that tolerogenic immune-modifying nanoparticles (TIMPs) encapsulating peptides/proteins is an effective therapeutic that induces antigen-specific tolerance to the encapsulated peptide/protein. The effectiveness of this therapeutic platform has been be demonstrated in multiple mouse models, as well as in a recently completed phase 2 double-blinded placebo-controlled clinical trial for the treatment of celiac disease. While previous EAE studies have utilized single peptides, the present study utilized a polypeptide containing the SJL/J mouse dominant encephalitogenic peptides (PLP139–151, PLP178–191, MBP84–104, and MOG92-10) linked together with intervening capsaicin S cleavage sites. The use of the multiple-linked myelin peptides was produced to achieve broader coverage of myelin-derived epitopes, which will be required for the treatment of MS. The present data show that this multiple-linked myelin peptide emulsified in CFA induced both CD4+ T cell responses and EAE in SJL/J mice similar to PLP139–151/CFA. Our data go on to show that treatment of SJL/J mice with multiple-linked myelin peptide TIMP inhibited both PLP139–151/CFA-induced R-EAE, as well as multiple-linked myelin peptide/CFA-induced EAE. Furthermore, treatment of SJL/J mice with multiple-linked myelin peptide TIMP significantly decreased TH17 cell responses and increased Tr1 cell responses. The present findings suggest that utilizing multiple-linked peptides may be clinically translatable for the treatment of autoimmune disease.
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Bronstein, J. M., R. Lallone, R. S. Seitz, G. W. Ellison, and L. W. Myers. "A humoral response to OSP in multiple sclerosis: A molecular mimic?" Multiple Sclerosis Journal 2, no. 5 (December 1996): 250. http://dx.doi.org/10.1177/135245859600200512.
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Oligodendrocyte-specifie protein (OSP) is a recently isolated novel protein found only in CNS laminar myelin and therefor is a good candidate as an autoantigen in patients with MS. In order to determine the humoral response in patients with MS. Westren blot analysis was performed on CSF from 6 patients with clinically stable relapsing MS (rMS) and 2 normal controls. All 6 of the CSF samples from rMS patients contained anti-OSP antibodies and none were detected in controls. Peptide mapping determined that the antigenic response was directed at a 7 amino acid peptide (OSP 114-120) which was 71% homologous with several common viral and bacterial proteins and 100% identical to the human OSP protein. ELISAs were performed using OSP 114-20 as antigen on a total 32 MS patints followed at UCLA, 53 MS patients from the National Neurological Rescarch Specimen Bank (NNRSB), and on 51 neurological control samples. Eighty % of UCLA rMS patients had an OSP ELISA reading above 0.55 OD units (median ± SD, 0.94 ± .35) while 0 of 14 CSF samples from HTLV-1 patients and normal controls had values above 0.55 units (0.28 ± .12; p<.01). Similar results were found in specimens from the NNRSB. No differences in anti-OSP titers were found in serum of MS and control patients. ELISAs performed on CSF samples using homologus viral peptieds as antigen (e.g. EBV, HSV HIV) showed a close correlation with anti-OSP 114-120 titers, and in some, the anti-viral titers far exceeded them. These data demonstrate a specific humoral response directed against a region of OSP in rMS patinets which cross reacts with several common viral peptides and suggests a possible role of molecular mimicry in the development of MS.
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Matsoukas, John M., Irene Ligielli, Christos T. Chasapis, Konstantinos Kelaidonis, Vasso Apostolopoulos, and Thomas Mavromoustakos. "Novel Approaches in the Immunotherapy of Multiple Sclerosis: Cyclization of Myelin Epitope Peptides and Conjugation with Mannan." Brain Sciences 11, no. 12 (November 29, 2021): 1583. http://dx.doi.org/10.3390/brainsci11121583.
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Multiple Sclerosis (MS) is a serious autoimmune disease. The patient in an advanced state of the disease has restrained mobility and remains handicapped. It is therefore understandable that there is a great need for novel drugs and vaccines for the treatment of MS. Herein we summarise two major approaches applied for the treatment of the disease using peptide molecules alone or conjugated with mannan. The first approach focuses on selective myelin epitope peptide or peptide mimetic therapy alone or conjugated with mannan, and the second on immune-therapy by preventing or controlling disease through the release of appropriate cytokines. In both approaches the use of cyclic peptides offers the advantage of increased stability from proteolytic enzymes. In these approaches, the synthesis of myelin epitope peptides conjugated to mannan is of particular interest as this was found to protect mice against experimental autoimmune encephalomyelitis, an animal model of MS, in prophylactic and therapeutic protocols. Protection was peptide-specific and associated with reduced antigen-specific T cell proliferation. The aim of the studies of these peptide epitope analogs is to understand their molecular basis of interactions with human autoimmune T-cell receptor and a MS-associated human leucocyte antigen (HLA)-DR2b. This knowledge will lead the rational design to new beneficial non-peptide mimetic analogs for the treatment of MS. Some issues of the use of nanotechnology will also be addressed as a future trend to tackle the disease. We highlight novel immunomodulation and vaccine-based research against MS based on myelin epitope peptides and strategies developed in our laboratories.
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Androutsou, Maria-Eleni, Agathi Nteli, Areti Gkika, Maria Avloniti, Anastasia Dagkonaki, Lesley Probert, Theodore Tselios, and Simona Golič Grdadolnik. "Characterization of Asparagine Deamidation in Immunodominant Myelin Oligodendrocyte Glycoprotein Peptide Potential Immunotherapy for the Treatment of Multiple Sclerosis." International Journal of Molecular Sciences 21, no. 20 (October 13, 2020): 7566. http://dx.doi.org/10.3390/ijms21207566.
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Mannan (polysaccharide) conjugated with a myelin oligodendrocyte glycoprotein (MOG) peptide, namely (KG)5MOG35–55, represents a potent and promising new approach for the immunotherapy of Multiple Sclerosis (MS). The MOG35–55 epitope conjugated with the oxidized form of mannan (poly-mannose) via a (KG)5 linker was found to inhibit the symptoms of MOG35–55-induced experimental autoimmune encephalomyelitis (EAE) in mice using prophylactic and therapeutic vaccinated protocols. Deamidation is a common modification in peptide and protein sequences, especially for Gln and Asn residues. In this study, the structural solution motif of deaminated peptides and their functional effects in an animal model for MS were explored. Several peptides based on the MOG35–55 epitope have been synthesized in which the Asn53 was replaced with Ala, Asp, or isoAsp. Our results demonstrate that the synthesized MOG peptides were formed to the deaminated products in basic conditions, and the Asn53 was mainly modified to Asp. Moreover, both peptides (wild type and deaminated derivative) conjugated with mannan (from Saccharomyces cerevisiae) independently inhibited the development of neurological symptoms and inflammatory demyelinating spinal cord lesions in MOG35–55-induced EAE. To conclude, mannan conjugated with a deamidated product did not affect the efficacy of the parent peptide.
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Bourdette, Dennis N., Yuan K. Chou, Ruth H. Whitham, Jane Buckner, Hi Jong Kwon, Gerald T. Nepom, Abigail Buenafe, et al. "Immunity to T Cell Receptor Peptides in Multiple Sclerosis. III. Preferential Immunogenicity of Complementarity-Determining Region 2 Peptides from Disease-Associated T Cell Receptor BV Genes*." Journal of Immunology 161, no. 2 (July 15, 1998): 1034–44. http://dx.doi.org/10.4049/jimmunol.161.2.1034.
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Abstract Vaccination with synthetic TCR peptides from the BV5S2 complementarity-determining region 2 (CDR2) can boost significantly the frequency of circulating CD4+ peptide-specific Th2 cells in multiple sclerosis (MS) patients, with an associated decrease in the frequency of myelin basic protein (MBP)-reactive Th1 cells and possible clinical benefit. To evaluate the immunogenicity of CDR2 vs other regions of the TCR, we vaccinated seven MS patients with overlapping BV5S2 peptides spanning amino acids 1–94. Six patients responded to at least one of three overlapping or substituted CDR2 peptides possessing a core epitope of residues 44–52, and one patient also responded to a CDR1 peptide. Of the CDR2 peptides, the substituted (Y49T)BV5S2-38–58 peptide was the most immunogenic but cross-reacted with the native sequence and had the strongest binding affinity for MS-associated HLA-DR2 alleles, suggesting that position 49 is an MHC rather than a TCR contact residue. Two MS patients who did not respond to BV5S2 peptides were immunized successfully with CDR2 peptides from different BV gene families overexpressed by their MBP-specific T cells. Taken together, these results suggest that a widely active vaccine for MS might well involve a limited set of slightly modified CDR2 peptides from BV genes involved in T cell recognition of MBP.
Dissertations / Theses on the topic "Sclerosi multipla peptides"
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Kissler, Stephan. "How transgenic T cells interpret encounter with peptide antigen." Thesis, University of Bristol, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.324380.
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Allen, Stephanie D. "Therapeutic peptidomimetic strategies for costimulation blockade in multiple sclerosis and transplantation / conformational peptide vaccines of the HER-2/neu dimerization loop are effective in inhibiting mammary tumor growth in vivo." Columbus, Ohio : Ohio State University, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1150479940.
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Kanthamneni, Naveen. "Development of Immunosupressant and Peptide Loaded Microparticles as Tolerogenic Vaccines for Treatment of Autoimmune Diseases." The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1331050212.
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Vargas, Sanchez Jeinny. "In vivo peptide biomarker screening for molecular imaging in eae neuroinflammation." Thesis, Bordeaux 2, 2013. http://www.theses.fr/2013BOR22102/document.
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Dans les maladies neurodégénératives comme la sclérose en plaques, la neuro-inflammation modifie l'activité de la barrière hémato-encéphalique (BHE) par des altérations cellulaires et moléculaires complexes. La caractérisation de tels changements moléculaires par une approche d'étiquetage in vivo justifie la recherche d’outils de ciblage fiables et de biomarqueurs. Les stratégies pour définir in vivo ces marqueurs sont cependant compliquées par la pléthore de molécules cibles accessibles, par l’intrication des régions atteintes au sein du tissu sain et par les altérations structurales potentielles des molécules cibles étudiées par histopathologie. Le but de ce travail est de rationaliser la découverte de biomarqueurs des altérations moléculaires dans les tissus par une stratégie de sélection in vivo de répertoires de phages présentant des peptides à leur surface (phage display), les ligands présents dans les deux répertoires (sain et pathologique) étant ensuite soustraits physiquement. Cette stratégie de soustraction (« PhiSSH ») permettant d’enrichir un répertoire en ligands spécifiques est d’un intérêt majeur dans le cas de répertoires complexes tels ceux obtenus dans des sélections in vivo.Nous présentons l'application de cette stratégie dans le modèle de rat de la sclérose en plaques, l’Encéphalomyélite Autoimmune Expérimentale (EAE), où les lésions disséminées dans le système nerveux central engendrent la sélection d’une grande quantité de clones s’associant au tissu sain, par comparaison avec les rats témoins en bonne santé. L'efficacité de la technique de soustraction a été contrôlée par séquençage massif des trois repertoires, «EAE», «SAIN», et «SOUSTRACTION». Plus de 95 % des clones communs aux répertoires EAE et contrôle sont absents du répertoire de la soustraction. Un ensemble de clones de phages et des peptides synthétisés chimiquement dessinés après l’analyse bioinformatique du répertoire de soustraction a été testé a) sur des tissus de rats EAE et sains et b) sur des cellules humaines en culture (HCMEC/D3) constituant un modèle de BHE, dans des conditions inflammatoires, (activation IL- 1ß) ou non activées. Un des clones et quatre peptide testés ont montré une association spécifique sur les cellules endothéliales de BHE dans des conditions inflammatoires. Pour identifier la cible d’un phage spécifique des lésions neuro-inflammatoires, nous avons mis en œuvre un procédé de création de liaison covalente entre ce phage et les protéines exprimées par des cellules de BHE cultivées en présence d’IL-1ß, puis effectué une analyse par spectométrie de masse. La galectine-1 est apparue comme une cible potential de ce phage. La découverte de biomarqueurs spécifiques de modifications moléculaires et cellulaires de régions inflammatoires disséminées dans les tissus sains, comme c’est le cas dans la plupart des pathologies présentant une activité neuro–inflammatoire, sera facilitée par l’utilisation de la stratégie de soustraction PhiSSH décrite dans ce documentIn neurodegenerative disorders like multiple sclerosis, neuroinflammation modifies the blood brain barrier (BBB) status by causing complex cellular and molecular alterations. Characterization of such molecular changes by an in vivo labeling approach is most challenging to generate reliable in vivo targeting tools and biomarkers. In vivo strategies to define such markers are, however, hampered by the plethora of the accessible target molecules, the vicinity of diseased target expression among healthy tissue and the potentially structural alterations of target molecules when studied by histopathology. The aim of this work is to streamline the biomarker discovery of pathological molecular tissue alterations by in vivo selection of phage displayed peptide repertoires that are further submitted to physical DNA subtraction (“PhiSSH”) of sequences encoding common peptides in both repertoires (HEALTHY and PATHOLOGY). The strategy of Subtraction allows thus the enrichment of clones specific for one repertoire and is of particular interest for complex repertoires produced by in vivo selection. We present the application of this strategy in the multiple sclerosis rat model, Experimental Autoimmune Encephalomyelitis (EAE) pathology, where target lesions are disseminated in the central nervous system (CNS) generating a large amount of clones binding to healthy tissue among the recovered repertoire clones binding to the lesions by comparison with healthy control rats. The efficiency of the subtraction was monitored by massive sequencing of the three repertoires, «EAE», «HEALTHY», and «SUBTRACTION». More than 95% of the clones common to EAE and Healthy repertoires were shown to be absent from the Subtraction repertoire. A set of randomly chosen clones and synthesized peptides from the EAE and subtraction repertoires were tested for differential labeling of a) diseased and healthy animal tissues and b) an in vitro BBB model, in IL-1ß challenged and resting control state culture human cells (hCMEC/D3). One of the phage clones and 4 chemically synthesized peptides showed specific binding to brain ECs in neuro-inflammatory conditions. Using a strategy of crosslinking of an EAE specific phage clone on protein targets expressed by IL-1ß activated ECs followed by mass spectrometry, we propose hypothetically Galectin-1 as a possible target of this phage. PhiSSH will be useful for in vivo screening of small peptide combinatorial libraries for the discovery of biomarkers specific of molecular and cellular alterations untangled with healthy tissues, as in most pathologies presenting neuroinflammatory activity
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Schirer, Alicia. "Les maladies neurodégénératives : étude de peptides modèles, de tissus cérébraux et de liquides céphalorachidiens par (micro)spectroscopie infrarouge et Raman." Thesis, Strasbourg, 2016. http://www.theses.fr/2016STRAF055/document.
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Les maladies neurodégénératives représentent un défi sociétal majeur. Trouver des outils pour mieux comprendre et diagnostiquer ces maladies est donc nécessaire. La spectroscopie infrarouge (IR) et Raman semblent être de bons candidats puisqu’elles peuvent caractériser l’état physiopathologique d’un échantillon. Le but de cette thèse a été d’appliquer ces méthodes à l’étude de peptides modèles, de tissus cérébraux et de liquides céphalorachidiens (LCR). Dans le cadre de l’étude des tissus cérébraux, la spectroscopie IR et Raman ont été couplées à la microscopie afin de combiner des informations spectrales et spatiales. Cela a permis de mieux comprendre la formation et le rôle des plaques amyloïdes dans la maladie d’Alzheimer (MA). Egalement, cela a permis de montrer l’intérêt d’utiliser ces méthodes dans des études futures pour suivre l’effet de différents traitements contre la sclérose en plaques. Concernant l’étude des LCR, la spectroscopie IR en mode ATR et la spectroscopie Raman exaltée de surface ont été utilisées afin de mettre en évidence des marqueurs spectroscopiques de la MA et de la maladie à corps de Lewy qui pourraient permettre un diagnostic plus précoce de ces maladies et un diagnostic différentiel entre ces deuxNeurodegenerative diseases represent a major societal challenge. So, it is necessary to develop new tools for a better understanding and diagnosing of these diseases. Infrared (IR) and Raman spectroscopies seem to be good candidates since they can characterize the physiopathological conditions of a biological sample. The purpose of this thesis was to apply these methods to the study of model peptides, brain tissues and cerebrospinal fluids (CSF). As a part of brain tissue analysis, IR and Raman spectroscopy were coupled to microscopy in order to combine spectral and spatial information. This methodology improved our understanding of the formation and the role of amyloid plaques in Alzheimer’s disease (AD). Moreover, it allowed to demonstrate the potential of these approaches in future studies on the effect of various treatments against multiple sclerosis. Concerning the study of CSF, IR-ATR and surface enhanced Raman spectroscopy were applied to identify spectroscopic markers of AD and Lewy body disease that could enable early diagnosis of these diseases and discrimination between them
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Becquet, Laurine. "Evaluation des effets thérapeutiques de neuropeptides contre la sclérose en plaques : les orexines, le vasoactive intestinal peptide, le pituitary adenylate cyclase-activating polypeptide et leurs analogues." Thesis, Normandie, 2018. http://www.theses.fr/2018NORMR071.
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La sclérose en plaques (SEP) est une maladie autoimmune inflammatoire et neurodégénérative du système nerveux central (SNC) chez le jeune adulte résultant d’une altération ciblée de la myéline. Les premiers symptômes de la SEP sont une détérioration cognitive, des vertiges, des douleurs, de la fatigue et une perte de la vision. En condition physiologique, les axones des neurones sont entourés par une gaine de myéline synthétisée par les oligodendrocytes permettant d’accélérer la vitesse de conduction des influx nerveux et de prévenir la mort neuronale. Le modèle expérimental le plus utilisé dans l’étude des mécanismes de la SEP est le modèle de l’encéphalomyélite autoimmune expérimentale (EAE). Après une immunisation contre la glycoprotéine oligodendrocytaire de la myéline 35-55 (MOG35-55), les lymphocytes T Cluster of differentiation (CD)4+ helper (Th)1 et Th17 auto-réactifs induisent une réponse inflammatoire aiguë à la périphérie puis migrent dans le SNC. Ils provoquent alors une réponse inflammatoire dirigée contre la myéline, avec l’intervention descellules myéloïdes. Cela aboutit à la destruction des gaines de myéline diminuant la vitesse de conduction des influx nerveux et une perte axonale, responsables des symptômes mentionnés précédemment. A l’heure actuelle, les traitements contre la SEP peuvent ralentir la progression de la paralysie et diminuer la sévérité ainsi que l’incidence des symptômes diminuant l’inflammation. En revanche, ils n’ont pas d’effets sur les formes progressives de la maladie au cours desquellesles processus neurodégénératifs s’amplifient et dominent ceux de l’inflammation. Il est donc nécessaire de trouver de nouvelles thérapies qui pourront à la fois bloquer l’inflammation et promouvoir la remyélinisation et la neurorégénération. Dans cette optique, de nouvelles cibles thérapeutiques ont émergé pour traiter la SEP : le Vasoactive Intestinal Peptide (VIP), le Pituitary Adenylate Cyclase-Activating Polypeptide (PACAP), l’orexine A, leurs récepteurs ainsi queleurs analogues. En effet, ces neuropeptides présentent des activités anti-inflammatoires et neuroprotectrices. Mes travaux de thèse ont porté sur l’étude des effets d’un agoniste de VPAC2, l’un des récepteurs de VIP et PACAP, et de l’orexine A sur les processus inflammatoires et neurodégénératifs dans le modèle d’EAE ainsi que dans le modèle toxique de la cuprizone (CPZ), induisant la mort des oligodendrocytes matures et la démyélinisation indépendamment des lymphocytes T. Après une immunisation contre la MOG35-55, un traitement systémique de court durée avec BAY55-9837, un agoniste de VPAC2, diminue la sévérité de l’EAE chronique en diminuant la réponse inflammatoire à la périphérie avec une baisse de l’activation lymphocytaire, de l’activité de présentation antigénique des cellules dendritiques et des monocytes ainsi qu’une modulation de la population des lymphocytes T régulateurs. Au niveau de la moelle épinière, l’infiltration descellules immunitaires est moindre et la proportion en microglie/macrophages est plus élevée après traitement par l’agoniste de VPAC2. De plus, BAY55-9837 diminue les processus de démyélinisation et favorise ceux de remyélinisation dans le modèle de la CPZ. En parallèle, l’administration intrapéritonéale à court terme de l’orexine A diminue drastiquement la sévérité de l’EAE chronique. Le traitement ne présente pas d’effet sur la phase d’immunisation de l’EAE mais limite la phase effectriceavec une diminution de l’infiltration des lymphocytes T CD4+, des médiateurs inflammatoires, de la démyélinisation, de l’astrogliose et de l’activation microgliale au niveau du SNC. Par contre, l’administration systémique de l’orexine A ne semble pas avoir d’effet sur les phases de démyélinisation et de remyélinisation au cours du modèle de la CPZMultiple sclerosis (MS) is a chronic autoimmune and neurodegenerative disease of the central nervous system (CNS). First MS symptoms are cognitive deterioration, dizziness, pain, fatigue and loss of vision. In physiological condition, the axons of neurons are surrounded by a myelin sheath synthesized by oligodendrocytes to accelerate the conduction velocity of nerve impulses and to prevent neuronal death. The most widely used experimental model of MS is the EAE model. After immunization against MOG35-55, self-reactive Th1 and Th17 cells induce an acute inflammatory response at the periphery and then migrate into the SNC. Then they induce an inflammatory response against myelin, with the intervention of myeloid cells. This results in the destruction of myelin sheaths decreasing the rate of conduction of nerve impulses and axonal loss, responsible for the aforementioned symptoms. Currently, MS treatments can slow the progression of paralysis and decrease the severity and the incidence of symptoms by targeting immune responses. However, these treatments have no effect on the progressive forms of the disease when the neurodegenerative processes amplify and dominate the inflammatory component. It is therefore necessary to find effective therapies that can both block inflammation and also promote remyelination and neuroregeneration.In this context, new therapeutic targets have emerged to treat MS: VIP, PACAP, orexin A, their receptors and their analogs. These neuropeptides have several effects such as anti-inflammatory and neuroprotective activities. My thesis works were focused on the effect of a VPAC2 receptor agonist, one of the three receptors of VIP and PACAP, and orexin A in inflammatory and neurodegenerative processes during MOG35-55-induced EAE model and toxic model using CPZ, which induces mature oligodendrocyte death and demyelination without the influence of lymphocytes.A short term and systemic treatment of BAY55-9837, a VPAC2 agonist, decreases chronic EAE severity with less activation of T lymphocytes and antigen presentation activities of dendritic cells and monocytes as well as Treg population modulation at the periphery. In the CNS, immune cell infiltration is reduced in VPAC2-treated mice compared to PBS-treated mice with an higher microglia/macrophage proportion. Moreover, VPAC2 agonist decreases demyelination processes and enhances remyelination during cuprizone model. In parallel, short term and intraperitoneal administration of orexin A decreases drastically the severity of chronic EAE. Orexin A treatment has no effect on immunization phase of EAE but limits effective phase with a lower infiltration of CD4+ T lymphocytes, inflammatory mediators, demyelination, astrogliosis and microglial activation in the CNS. In contrast, systemic administration of orexin A seems to have no effect during demyelination and remyelination phases in CPZ model
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Mazzoleni, Antonio. "Glucosylated peptides in autoimmune diseases: synthetic strategies and application to antibody detection and capture." Doctoral thesis, 2020. http://hdl.handle.net/2158/1197513.
Full textAbstract:
The main purpose of this thesis was to develop peptide probes to detect and isolate specific and high affinity antibodies from sera of patients suffering from multiple sclerosis (MS). We selected a di-glucosylated adhesin HMW1 peptide as the shortest sequence up to now able to compete with the highest affinity with anti-N(Glc) IgM binding. 40 kDa dextran was modified with propargyl groups and used as a scaffold to conjugate by CuAAC the di-glucosylated peptide. This novel polymeric structure was proven to dramatically increase binding potency of IgGs and IgMs in MS sera. Abs from a representative MS serum, were successfully purified on a sepharose resin specifically modified with the adhesin peptide-dextran conjugate, as confirmed by ELISA. This result appears promising as a proof-of-concept of the selective removal of circulating autoantibodies (possibly perpetuating nonself recognition) that could likely lead to develop a specific apheresis-based device.
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Sibilla, Antonio. "Use of the non-peptidic Nerve Growth Factor mimetic MT2 to activate TrkA and TrkB receptors: a therapeutic tool in Multiple Sclerosis." Doctoral thesis, 2018. http://hdl.handle.net/2158/1178147.
Full textAbstract:
MT2 is a novel Nerve Growth Factor peptidomimetic, able to exert its effects binding the Tropomyosin receptor kinase A (TrkA) and B (TrkB), the high affinity receptor for Nerve Growth Factor (NGF) and Brain-derived neurotrophic factor (BDNF). These latter molecules are part of neurotrophins family, and they have been tested in pharmacology for their trophic function: despite this, their polypeptide nature forced to use very invasive way of administration, making them virtually impossible to use for therapeutic purposes.
Unlike them, MT2 is a non-peptidic smaller molecule with an optimal pharmacokinetic that showed to be effective in activating the MAPK/ERK pathway. Through this pathway, MT2 demonstrated to trigger an anti-apoptotic signal both in in vitro model of Alzheimer's disease (AD) based on NGF deprivation of rat hippocampal neurons (Scarpi D et al. 2012) and in in vivo experimental models of acute global ischemia in gerbils, where it prevented death of hippocampal neurons. Considering this, our aim was to understand if MT2 could be a pharmaceutical tool for inflammatory insult in central nervous system (CNS) exploiting appropriate models.
First, we set up an in vitro spinal cord organotypic culture during an induced inflammatory stress by a pro-inflammatory cytokines cocktail: in this model we proved that MT2 is able keep unchanged any synaptic alterations. This effect seems to be mediated by the activation of classical NGF neurotrophic pathways kinases-driven, triggered by the bound of MT2 with TrkA and TrkB. These positive results were entirely due to an effect on CNS cells, because the absence of immune system mediators in this model.
These positive results led us to investigate whether MT2 could limit inflammatory events in central nervous system (CNS), setting up Experimental Autoimmune Encephalomyelites (EAE) MOG35-55-induced experiments. We treated animals during acute and chronic stages of disease: MT2 demonstrated to give beneficial effects treating animals at early stage of disease, limiting the classical hallmarks of disease. In fact, MT2-treated animals showed significant lower clinical signs in vivo and less presence of infiltrates and demyelinated areas in spinal cord, as demonstrated by ex vivo experiments. These effects resulted to be in charge of TrkA pathway activation. Moreover, we investigated if such effects could involve immune system cells, carrying on treatment on preclinical phase of EAE: ex vivo experiments results showed a significant lower production of IFN-γ by T-cells isolated from lymph nodes of treated animals, compared to controls, attesting a potent anti-inflammatory effect on immune system cells to MT2.
Last, we tested the possible beneficial effect of MT2 in limiting demyelination and promoting the remyelination in in vivo Cuprizone model. The drug demonstrated its inability in counteracting a non-immune cells-driven insult: toxic event in demyelination were not limited and, even, the peptidomimetic showed to worsen myelin conditions during the remyelinating phase of this model.
Considering everything in the whole, MT2 showed a neuroprotective its ability in narrowing the pro-inflammatory events on several neuroinflammatory models. The drug demonstrated to act both on immune system and on CNS cells, influencing the classical neurotrophic pathway activation. Despite this, it showed an adverse effect on toxic demyelination model, demonstrating that double specificity for TrkA and TrkB in absence of immune system involvement could possibly a harmful feature.
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Dargahi, Narges. "Immune modulation using probiotics and multiple sclerosis peptides." Thesis, 2019. https://vuir.vu.edu.au/41847/.
Full textAbstract:
Changes in physiological, immunological and gut microbiome can lead to a range of chronic conditions in humans. The ‘hygiene hypothesis’ identifies the increasing trend of immune-mediated disorders to possibly be a consequence of intestinal dysbiosis, that in turn results in a dysfunctional immune system leading to conditions such as, eczema, asthma, allergies and autoimmune diseases. Therefore, utilization of beneficial probiotic bacteria can increase their abundance within the gastrointestinal lumen, and subsequently modulate immune cells, such as, T helper (Th)-1, Th2, Th17, regulatory T (Treg) cells, B cells, macrophages, dendritic cells and monocytes. Modulation of immune cells are directly related to human health and pathogenesis of immune disorders. Chapter 1a describes the cross talk between probiotics and the gastrointestinal immune system, and their effects in relation to inflammatory bowel disease, multiple sclerosis (MS), allergies and atopic dermatitis.
MS is one of the debilitating autoimmune disease of the central nervous system which has been increasing during the past decades. MS severely affects patients’ health, work and quality of life, and its treatment has changed over the last 20 years. In chapter 1b the immunopathology of MS and various available treatments have been investigated. As all the MS immunotherapeutic drugs target relapsing remitting MS (RRMS), in particular developing a treatment for progressive forms of MS is a medical challenge and medical specialists and clinicians are in constant battle with serious treatment challenges for MS. Although β- interferons 1a or 1b and glatiramer acetate are accounted as the most commonly used injectable disease modifying therapies in RRMS, however, one of the major challenge of these types of therapies has been the lack of devotion to treatment among MS patients, with approximately 50% of patients ceasing their therapy plan within the first year. This chapter revisits the basics of the immune-pathophysiology of MS to gain insights in the development of innovative improved drug treatments and presents current drug treatments and new and emerging immune modulating approaches for the immunotherapy of MS. This chapter provides groundwork for vaccine (or immune modulation) development research and the investigation of new potential vaccines (immune modulators) against MS which are used in chapters 5a and 5b.
Backtracking probiotics beneficial effects to the host that occur through their contribution to the development and maintenance of a healthy immune system, tracked the steps to the use of some probiotics in the food industry as starter or secondary starter cultures to ferment dairy products. These probiotics include Streptococcus thermophilus (ST); in chapter 2, ST1275, ST285 and ST1342 bacteria were used to determine their modulatory effects on U937 human promonocytic cell line which exhibited differential cytokine induction, in particular, increased secretion of anti-inflammatory IL-4 and IL-10 cytokines were noted. ST also stimulated an increase in the production of CXCL8 and GM-CSF, as well as expression of cell surface markers, CD11c, CD86, C206, CD209, MHC-1. ST285 was determined the most potent probiotic, therefore was considered to investigate further in chapters 3, 4 and 6. The main objective of next study was to assess modulatory and anti-inflammatory properties of ST285 using human peripheral blood mononuclear cells (PBMC) from healthy donors. To fulfil this objective, modifications in the mRNA expression of genes related to innate and adaptive immunity were assessed and results showed strong immune modulatory effects of ST285 to human PBMC with an array of anti-inflammatory properties. ST285 reduced mRNA expression of IL-18, IFNγR1, CCR5, CXCL10, TLR-1, TLR-2, TLR-4, TLR-8, CD14, CD40, CD86, C3, GATA3, ITGAM, IRF7, NLP3, LYZ, TYK2 and IFNR1. ST285 upregulated IL- 1α, IL-1β, IL-6, IL-8, IL-10, IL-23, IFNγ, TNFα, CSF-2 to human PBMC; no changes to mRNA expression of IFNA1, IFNB1, IL-4, IL-5, IL-13, CCL2, CCL5, CCL8, CCR4, CCR8, CXCR3, TLR-3, TLR-5, TLR-6, TLR-9, CD4, CD80, FOXP3, STAT3, CD40LG, HLA-A, HLA-E and RORC were noted. These data demonstrated a predominant anti-inflammatory profile exhibited by ST285, hence, ST285 was validated for further investigation on human monocytes.
Some of the beneficial effects attributed to probiotics may be through modulation of the immune system; the effect of ST285 to human monocytes was assessed and a range of immune modulating effects of ST285 by human monocytes was demonstrated. This included significant downregulation in the mRNA expression of IL-1R, IL-18, IFNγR1, IFNαR1, CCL2, CCR5, TLR-1, TLR-2, TLR-4, TLR-5, TLR-6, TLR-8, CD14, CD86, CD4, ITGAM, LYZ, TYK2, IFNR1, IRAK-1, NOD2, MYD88, ITGAM, SLC11A1, and significant upregulation in the mRNA expression of IL-1α, IL-1β, IL-2, IL-6, IL-8, IL-23, IFNγ, TNFα, and CSF-2. ST285 is used in the dairy industry, survives during cold storage, well tolerates upon ingestion, and their consumption may have beneficial effects with potential implications in inflammatory and autoimmune disorders, such as, multiple sclerosis.
In order to determine a suitable autoimmune setting to investigate the effects of ST285 in an animal model, it was required to revisit MS treatments to determine the effects of recently developed agonist and antagonist MS vaccines. Encephalitogenic T cells are greatly implicated in the pathogenesis of MS, stimulation of these T calls is triggered by the formation of a tri- molecular complex among the human leukocyte antigen (HLA), an immunodominant myelin basic protein (MBP) epitope, and the T cell receptor (TCR). This next study (chapter 5) concentrated on the rational design and synthesis of non-peptide mimetic molecules, based on the immunodominant MBP83–96 epitope that is recognized by the TCR in complex with HLA, with a focused attention on the inhibition of the tri-molecular complex formation which can consequently lead to the inhibition of proliferation of activated T cells. In view of the interactions between the TCR and the HLA-MBP83–96 complex, a structure-based pharmacophore model was generated and the newly candidate molecules were obtained through the ZINC database, six molecules were synthesized and further evaluated in vitro as TCR antagonists. Analogues 15 and 16 were able to inhibit the stimulation of T cells by the immunodominant MBP83–99 peptide from immunized mice to some extent, and to a lesser degree by analogues 17 and 18 and then by analogue 19, presenting the lead compounds 15 and 16 may be used for immunotherapy against MS. In addition in chapter 5b, the immune modulatory effects of MBP83-99 peptide conjugated or not conjugated to carrier mannan, in either linear or cyclic forms were determined. It was shown that MBP83-99 modulated the immune responses in SJL/J immunized mice which resulted in cytokine secretion by immunized spleen cells which was protective in an experimental autoimmune encephalitis model and protection against axonal spinal damage. Molecular modelling was used to gain insights into the binding mode of the peptide to MHC class II.
In the chapter 6, the effects of ST285 to agonist MBP83-99 peptide immunized mouse spleen cells was determined. Agonist peptide induced a Th1 profile, however in the presence of ST285 a significant increase in the expression of anti-inflammatory IL-4, IL-5, IL-10 cytokines,and decreased pro-inflammatory IL-1β and IFN-γ were noted. Regular consumption of probiotic bacteria such as ST285 in the form of capsules, fermented food or dairy products may therefore be beneficial in the management and treatment of autoimmune diseases such as multiple sclerosis. Consumption of probiotics contributes to a healthy microbiome of the GIT leading to many health benefits. They also contribute to the modulation of the immune system and are becoming popular for the treatment of a number of immune and inflammatory diseases.
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Δεράος, Σπύρος. "Σχεδιασμός και σύνθεση αναλόγων επιτόπων της μυελίνης καθώς και αναλόγων της Β αλυσίδας του υποδοχέα της ιντερλευκίνης-2 : μελέτη δομής - βιολογικής δραστηριότητας." Thesis, 2003. http://nemertes.lis.upatras.gr/jspui/handle/10889/3451.
Full textBook chapters on the topic "Sclerosi multipla peptides"
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Ebringer, Alan. "Antibodies to Prion and Acinetobacter Peptide Sequences in Bovine Spongiform Encephalopathy." In Multiple Sclerosis, Mad Cow Disease and Acinetobacter, 79–86. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-02735-7_10.
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Ebringer, Alan. "Antibodies to Acinetobacter Peptide Sequences Resembling Myelin and Neurofilaments in Multiple Sclerosis Patients." In Multiple Sclerosis, Mad Cow Disease and Acinetobacter, 97–107. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-02735-7_12.
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Ebringer, Alan. "Antibodies to Short Synthetic Acinetobacter and Pseudomonas Peptide Sequences Resembling Myelin and Neurofilaments in Multiple Sclerosis Patients." In Multiple Sclerosis, Mad Cow Disease and Acinetobacter, 119–29. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-02735-7_14.
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Kurnellas, Michael P., Jonathan B. Rothbard, and Lawrence Steinman. "Self-Assembling Peptides Form Immune Suppressive Amyloid Fibrils Effective in Autoimmune Encephalomyelitis." In Emerging and Evolving Topics in Multiple Sclerosis Pathogenesis and Treatments, 221–32. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/7854_2015_377.
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Carotenuto, Alfonso, Armida Di Fenza, Elena Nardi, Anna M. Papini, and Paolo Rovero. "Conformational Studies of a Glycopeptide Recognized with High Affinity by Autoantibodies in Multiple Sclerosis." In Peptides: The Wave of the Future, 340–41. Dordrecht: Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-010-0464-0_156.
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Brocke, S. "T Cell Receptor Peptides for the Vaccination Therapy of Multiple Sclerosis." In Therapeutic Vaccination Strategies, 167–79. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-662-04183-3_11.
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Blalock, J. Edwin. "Neuroendocrine Peptide Hormones and their Receptors as Endogenous Components of the Immune System." In Cellular and Humoral Immunological Components of Cerebrospinal Fluid in Multiple Sclerosis, 443–51. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4899-5348-3_51.
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Arnon, Ruth, Michael Sela, and Rina Aharoni. "Peptides and Polypeptides as Immunomodulators and Their Consequential Therapeutic Effect in Multiple Sclerosis and Other Autoimmune Diseases." In Peptide Drug Discovery and Development, 313–35. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2011. http://dx.doi.org/10.1002/9783527636730.ch15.
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Bielekova, B., and R. Martin. "Specific Immunotherapy of Multiple Sclerosis by Altered Peptide Ligands — Risk or Benefit?" In New Concepts in Pathology and Treatment of Autoimmune Disorders, 69–87. Berlin, Heidelberg: Springer Berlin Heidelberg, 2001. http://dx.doi.org/10.1007/978-3-662-04450-6_5.
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Tzoupis, Haralambos, and Theodore Tselios. "In Silico Drug Design: Non-peptide Mimetics for the Immunotherapy of Multiple Sclerosis." In Methods in Molecular Biology, 33–47. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8630-9_3.
Full textConference papers on the topic "Sclerosi multipla peptides"
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Vezenkov, Lyubomir, Borislav Anchev, Ivanka Kostadinova, Kristian Fidanov, Daniela S. Tsekova, Nikolay G. Vasilev, and Nikolai D. Danchev. "New 4-Aminopyridine derivatives containing peptide fragment designed for the treatment of Alzheimer disease and multiple sclerosis." In 35th European Peptide Symposium. Prompt Scientific Publishing, 2018. http://dx.doi.org/10.17952/35eps.2018.241.
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Casoria, Michele, Paolo Rovero, Gianni Cardini, Marina Macchiagodena, Anna Maria Papini, Claudia Andreini, and Marco Pagliai. "From a Bioinformatic Approach to Synthetic Conformational Peptide Epitopes to Disclose Molecular Mechanism of Aberrant Glucosylation in Multiple Sclerosis." In 36th European Peptide Symposium. The European Peptide Society, 2022. http://dx.doi.org/10.17952/36eps/36eps.2022.237.
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