Дисертації з теми "Chemokine biology"
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Maru, Seema V. "The role of chemokines and chemokine receptors in astrocytes and astrocytoma biology." Thesis, Open University, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.427496.
Повний текст джерелаMillette, Roxanne. "The effect of chemokine CCL19 on B lymphocytes /." Thesis, McGill University, 2002. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=79051.
Повний текст джерелаFinley, Matthew James. "Molecular Basis for Kappa-Opioid Regulation of Chemokine Receptor Function." Diss., Temple University Libraries, 2009. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/62878.
Повний текст джерелаPh.D.
Opioid receptor-mediated regulation of chemokine receptors is vital for the host immune response, development, and neurological function. Previous studies have demonstrated that the kappa opioid receptor (KOR) activation results in decreased infectivity of human immunodeficiency virus 1 (HIV-1) in human peripheral blood mononuclear cells (PBMCs). We have found this effect is due to down-regulation of the major HIV-1 co-receptors, CCR5 and CXCR4. Using molecular techniques, CCR5 and CXCR4 mRNA levels drop dramatically following KOR activation. To dissect the mechanism involved, we used transcription factor binding arrays and compared control cell extracts to KOR activated cell extracts. We determined that the interferon regulatory factors (IRFs) and signal transducers and activators of transcription (STATs) could be involved in the KOR-mediated repression of CCR5 and CXCR4 transcription and protein expression. Using chemical inhibitors and small interfering RNA (siRNA) molecules, we determined that JAK2, STAT3, and IRF2 are critical members of this signal transduction pathway. The understanding of these particular mechanisms should prove to be beneficial for the development of potential pharmacological agents targeted at HIV-1 binding and infection since virus infection requires expression of the co-receptors CXCR4 and CCR5. Understanding the molecular basis for KOR-induced inhibition of co-receptor expression may provide a basis for the development of KOR agonist-based therapeutics to treat individuals infected with HIV.
Temple University--Theses
Zhu, John Z. "Sulfotyrosines impart ligand specificity in a chemokine receptor model system." [Bloomington, Ind.] : Indiana University, 2009. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3380144.
Повний текст джерелаTitle from PDF t.p. (viewed on Jul 20, 2010). Source: Dissertation Abstracts International, Volume: 70-12, Section: B, page: 7377. Advisers: Martin J. Stone; Carl E. Bauer.
Tiplady, Eleanor Margaret. "Expression and modulation of atypical chemokine receptors on epithelial cells." Thesis, University of Glasgow, 2018. http://theses.gla.ac.uk/30618/.
Повний текст джерелаRandolph-Habecker, Julie. "The expression and function of the human cytomegalovirus encoded beta-chemokine receptor homolog, US28 /." The Ohio State University, 1998. http://rave.ohiolink.edu/etdc/view?acc_num=osu148795159550182.
Повний текст джерелаCook, Sarah Louise. "The role of CC-chemokine receptor-like 2 in the B cell response." Thesis, University of Birmingham, 2015. http://etheses.bham.ac.uk//id/eprint/5645/.
Повний текст джерелаMukhi, Sumedha. "Effects of Chronic Morphine Administration on Cytokine & Chemokine Protein and Gene Expression." Master's thesis, Temple University Libraries, 2012. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/214787.
Повний текст джерелаM.S.
Chemokine and chemokine receptors play a major role in HIV-1 infectivity, and their expression can be modulated by opioid drugs of abuse, further implicating a role for these drugs in altering HIV-1 susceptibility. Several of the opioid agonists including morphine and heroin impair resistance to a variety of infectious agents including HIV-1 by modulating both innate and acquired immune responses. The aim of my thesis is to understand whether chronic morphine administration alters the expression of pro-inflammatory cytokines and chemokines. Since there are limited reports in the literature describing the effects of chronic opioid administration on immune competence, a macaque model was devised to analyze the immune system following chronic morphine administration. My results show that animals receiving morphine exhibit enhanced proinflammatory CXCL8 protein expression in response to stimulation with various Toll Receptor (TLR) ligands. This result was observed in responses to either the combination of LPS and IFNγ, or with the TLR ligand peptidoglycan. These results suggest that chronic morphine administration increases immune system responsiveness. We extended these studies on opioid-induced signaling and gene expression in human subjects and observed that opioid treatment induces the expression of CXCL10, TLR4, and the aryl hydrocarbon receptor (AHR) in leukocytes early in response to treatment. In sum, I have shown that opioid agonists modulate important immune-response genes, and these genes are important for the generation of antimicrobial immunity.
Temple University--Theses
Jung, Jaeho. "Cytokine and chemokine gene expression during influenza virus infection, and the effects of restraint stress /." The Ohio State University, 1996. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487942182322557.
Повний текст джерелаQu, Yiding. "Role of non-signaling (decoy) chemokine receptors in regulating cell migration: the mathematical model." Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=114337.
Повний текст джерелаLes chimiokines appartiennent à une importante famille de ligands chimiotactiques qui guident la direction migratoire des cellules. Sur une cellule-cible, des récepteurs spécifiques à une chimiokine donnée répondent à un gradient du ligand, provoquant la migration cellulaire vers le signal avec une concentration croissante. Cependant, quelques récepteurs pouvant liés des chimiokines ont récemment été identifiés comme muets (leurre) parce que la liaison du ligand ne stimule pas de signalisation mesurable dans la cellule. La fonction de ces récepteurs-leurres n'est pas connue actuellement.Nous avons émis l'hypothèse que l'interaction des chimiokines à ces récepteurs-leurres contribue à maintenir un gradient de ligand plus prononcé et donc stimule les cellules à migrer. Afin de tester cette hypothèse, nous avons en premier comparé l'expression de récepteurs signalant et de récepteurs-leurres pour un même ligand, quand des cellules deviennent métastatiques. En utilisant des bases de données publiques sur l'expression des gènes dans des échantillons de prostate normale, de carcinomes prostatiques, et de métastases prostatiques, nous avons remarqué que l'expression des récepteurs-leurres CCX-CKR et OPG est augmentée dans les cellules métastatiques lorsque comparée avec les cellules de prostate normales. Nous avons aussi trouvé une corrélation positive avec les niveaux d'expression des récepteurs signalants CCR7 et RANK. Par la suite, nous avons développé un modèle mathématique qui prédit la dynamique des concentrations de chimiokines, l'expression des récepteurs signalants, des récepteurs-leurres, et des mouvements de la cellule résultants. Nous avons tout d'abord utilisé ce modèle afin de prédire comment des cellules exprimant seulement des récepteurs signalant migrent vers la source du ligand selon sa concentration. En présence de faibles concentrations de ligand, la migration cellulaire augmente proportionnellement à l'augmentation de la concentration du ligand. Cependant, à des concentrations plus élevées dépassant la capacité de liaison du récepteur signalant, une augmentation subséquente diminue la distance migrée par la cellule. L'expression concomittante de récepteurs-leurres améliore la vitesse et la distance de la migration cellulaire lorsque la concentration du ligand est élevée. Cette étude suggère donc que les récepteurs-leurres des chimiokines contribuent au gradient chimiotactique et augmentent la migration des cellules.
Godbout, Marianne. "Role of toll-like receptor 4 in Leishmania-induced chemokine gene expression and inflammatory response." Thesis, McGill University, 2005. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=82242.
Повний текст джерелаHappel, Christine. "Molecular Basis for Mu-Opioid Regulation of Chemokine Gene Expression." Diss., Temple University Libraries, 2009. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/28438.
Повний текст джерелаPh.D.
Opioid receptor modulation of pro-inflammatory cytokine production is vital for host defense and the inflammatory response. Previous results have shown the mu-opioid receptor (MOR) selective agonist, DAMGO, has the capacity to increase the expression of the pro-inflammatory chemokines, CCL2/MCP-1, CCL5/RANTES and CXCL10/IP-10 in peripheral blood mononuclear cells (PBMCs). We have shown that MOR activation is able to induce the expression of TGF-β, and TGF-β appears to be required for induction of CCL5 following MOR activation. This work suggests a novel role for TGF-β in the inflammatory response. NF-κB is a transcription factor that plays a pivotal role in inflammation and the immune response. We have found that NF-kB inhibitors can prevent the MOR-induced activation of CCL2 and CCL5, and that the NF-kB subunit, p65, is phosphorylated at serine residues 311 and 536 in response to μ-opioid receptor activation. In vivo, DAMGO administration can induce binding of p. 65 to the enhancer region of the CCL2 promoter. Furthermore, we demonstrate that PKCζ is phosphorylated following DAMGO-induced MOR activation and, is essential for NF-kB activity as well as CCL2 expression and transcriptional activity. In conclusion, these data suggest a pro-inflammatory role for MOR which involves NF-κB activation and PKCζ as well as a novel role for TGF-β as a regulator of pro-inflammatory chemokines.
Temple University--Theses
Eshaque, Shathi. "Functional Characterization of Rainbow Trout (Oncorhynchus mykiss) Chemokine 2 (CK-2)." Thesis, University of Waterloo, 2006. http://hdl.handle.net/10012/1271.
Повний текст джерелаThrough genomic PCR on several outbred individuals it was shown that CK-2. 1 is an allele of CK-2 but not a separate gene. Reverse transcriptase (RT) PCR analysis revealed an increased level of transcript both CK-2 and CK-2. 1 in response to phytohaemagglutinin (PHA) stimulation of head kidney leukocytes (HKL) and peripheral blood leukocytes (PBL) collected from fish with different allelic distributions. Similar results were also observed in the rainbow trout macrophage/monocyte cell line, RTS11. Moreover, an anti-CK-2 antiserum was developed in rabbits, which cross-reacted with CK-2. 1. This newly produced antibody was used to determine the protein expression levels in PHA stimulated rainbow trout tissues. RT-PCR was also performed on the same tissues in order to examine the transcript expression. Rainbow trout with both CK-2 and CK-2. 1 were used for this experiment. An overall decreasing pattern of transcript (both CK-2 and CK-2. 1) was observed in brain and HK over 24 hours, while protein was still detected at 24 hours post stimulation. However, in spleen the CK-2 transcript showed a slight upregulation at 4 hours post stimulation along with a very little or no CK-2. 1 expression, although no protein was detected in spleen. Liver showed a very low level of CK-2 and CK-2. 1 transcript at 8 hours post stimulation; while protein was again detected at 24 hours post stimulation. In addition, the sizes of the proteins found in different tissues were larger than expected (≤30 kDa for CK-2 or ≤35 for CK-2. 1), perhaps due to the presence of extensive O-glycosylation at the mucin stalk of the protein.
A chemotaxis assay was carried out, which is the definitive assay for chemokine activity. This assay showed migration of peripheral blood leukocytes across a membrane with 5µm pores toward CK-2 at an optimal concentration of 500ng/ml (17nm). Moreover, by pre-treating the recombinant chemokine with the polyclonal antisera, it was shown that the chemokine was actually causing the chemotactic activity. Pre-treatment of the cells with pertussis toxin, an inhibitor of G-protein signalling inhibited the migration of PBLs, established the fact that CK-2 caused chemotaxis by binding to a 7 transmembrane, G-coupled receptor just like all other known chemokines. Interestingly, CK-2 was also shown to attract RTS-11 cells.
Overall, the above findings indicate that CK-2 is functionally a chemokine with two very different alleles in rainbow trout. It is probably heavily O-glycosylated and different tissues express different sizes of the protein. This is only the second functional study of a fish chemokine.
Heinisch, Silke. "Chemokine interactions with the serotonin and opioid systems: anatomical and electrophysiological studies in the rat brain." Diss., Temple University Libraries, 2008. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/9181.
Повний текст джерелаPh.D.
Chemokines, immune proteins that induce chemotaxis and adhesion, and their G-protein coupled receptors distribute throughout the central nervous system (CNS), regulate neuronal patterning, and mediate neuropathology. These chemo-attractant molecules may provide a neuro-immune "link" by regulating CNS systems. The purpose of this study was to investigate the interactions of specific chemokines, stromal cell-derived factor (SDF)-1a/CXCL12, and fractalkine/CX3CL1, and their receptors, CXCR4 and CX3CR1, with the serotonin (5-hydroxytryptamine; 5-HT) and opioid systems using anatomical and electrophysiological techniques in the rat brain. In the serotonin dense midbrain raphe nuclei (RN), SDF-1a, CXCR4, fractalkine and CX3CR1 co-localize over 70% with 5-HT neurons. CX3CR1 also localizes to microglia in the RN and hippocampus. Functionally, SDF-1a (10 nM) increases spontaneous inhibitory postsynaptic current (sIPSC) frequency and evoked IPSC (eIPSC) amplitude, while decreasing paired-pulse ratio (PPR) selectively in 5-HT neurons, thus stimulating presynaptic GABA release at these neurons. Alternatively, fractalkine (10 nM) increases sIPSC and eIPSC amplitude without changing PPR selectively in 5-HT neurons, thereby elevating the postsynaptic GABA receptor number or sensitivity. These results are dose-dependent and receptor-mediated. Chemokine interactions with serotonin, a neurotransmitter regulating mood, may lead to therapies for depression comorbid with immune diseases. Additional immunohistochemical analysis in the brain shows CXCR4 and CX3CR1 neuronal co-localization with the mu-opioid receptor (MOR) in the hippocampus, cingulate cortex, periaqueductal grey (PAG), nucleus accumbens, ventral tegmental area, globus pallidus, but not in the striatum or habenular nuclei, suggesting region specific receptor interactions. Electrophysiological recordings following morphine, SDF-1?? or fractalkine in vitro treatment reveal morphine (10 ?M)-mediated hyperpolarization of the membrane potential and reduction of the input resistance of PAG neurons, however, SDF-1??and fractalkine at 10 nM do not impact either parameter. In combination, SDF-1? inhibits morphine's actions in all PAG neurons tested, and fractalkine blocks morphine-mediated changes in 60% of PAG neurons examined. Thus, CXCR4 as well as CX3CR1, although less consistently, both appear to desensitize MOR at the neuronal level. Chemokine-opioid receptor interactions may mediate novel mechanisms to treat neuro-inflammatory pain and opiate abuse. The combined anatomical and electrophysiological results support chemokines as neuromodulatory proteins that may provide communication between the nervous and immune systems.
Temple University--Theses
Rojas-Rudolph, Isolde Gina. "Stress modulation of susceptibility to wound infection : effects on Leukocyte Trafficking and Chemokine Gene Expression during Cutaneous Wound Healing /." The Ohio State University, 2001. http://rave.ohiolink.edu/etdc/view?acc_num=osu1486474078047403.
Повний текст джерелаKontolemos, Mario. "Chemokine receptors on airway epithelial cells and their potential role in regulating mucin production." Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=78396.
Повний текст джерелаThe results of this study show that chemokine receptors are present on airway epithelial cells and that chemokines may act as a stimulus for epithelial cell mucin gene expression. Our novel finding that several CC chemokines upregulate the expression of MUC5AC mRNA might be an important mechanism regulating airway epithelial cell phenotype and function under conditions of inflammation in asthma.
Crisman, Jacqueline M. "Identification of amino acids that are responsible for the binding of macrophage inflammatory protein-1 [alpha] to the ckr1 chemokine receptor /." The Ohio State University, 1997. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487948158625889.
Повний текст джерелаGuan, Ping. "Identification, genomic structure, and functional studies of the human novel CC chemokine MIP-4, and the cloning of the murine homologue /." The Ohio State University, 1998. http://rave.ohiolink.edu/etdc/view?acc_num=osu148795320428111.
Повний текст джерелаCoke, Christopher James. "Cannabinoid Receptor 2 and C-X-C Chemokine Receptor 4 Interact to Abrogate CXCL12-Mediated Cellular Response." DigitalCommons@Robert W. Woodruff Library, Atlanta University Center, 2017. http://digitalcommons.auctr.edu/cauetds/76.
Повний текст джерелаPadovani-Claudio, Dolly Ann. "FUNCTIONAL ANALYSES OF THE CHEMOKINE RECEPTOR CXCR2 IN THE NORMAL AND DEMYELINATED ADULT CENTRAL NERVOUS SYSTEM." Case Western Reserve University School of Graduate Studies / OhioLINK, 2006. http://rave.ohiolink.edu/etdc/view?acc_num=case1152193193.
Повний текст джерелаPaccione, Kristin E. "Cytokine and Chemokine Profiles in a Rat Model of Hemorrhagic Shock after Immuno-Modulation by Androstenetriol." VCU Scholars Compass, 2005. http://hdl.handle.net/10156/2049.
Повний текст джерелаWendt, Emily Rose. "The role of CCL25 and CCR9 in intestinal inflammation." Thesis, University of Oxford, 2013. http://ora.ox.ac.uk/objects/uuid:c8413dcb-4861-4afd-ae13-5cb88935e54d.
Повний текст джерелаKramer, Ryan M. "Molecular Signature Characterization of Select Agent Pathogen Progression." University of Cincinnati / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1394725717.
Повний текст джерелаBurgoyne, Paul. "Improved dendritic cell therapy for cancer by enhancing in vivo lymph node migration using a novel chemokine-based sorting method." Thesis, University of Glasgow, 2019. http://theses.gla.ac.uk/39056/.
Повний текст джерелаAbhyankar, Vrushali Pavan. "The chemokine and cytokine responses of a keratinocyte, dendritic cell, and T-cell co-culture model treated with P. gingivalis hemagglutinin B (HagB)." Thesis, University of Iowa, 2016. https://ir.uiowa.edu/etd/2033.
Повний текст джерелаBenson, Bryan Lauck. "Mechanobiology of Leukocyte Adhesion." Case Western Reserve University School of Graduate Studies / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=case1537210425881461.
Повний текст джерелаLemma, S. (Siria). "Migration and adhesion associated molecules in lymphoma biology and their potential roles as biomarkers." Doctoral thesis, Oulun yliopisto, 2017. http://urn.fi/urn:isbn:9789526216041.
Повний текст джерелаTiivistelmä Lymfoomat ovat heterogeeninen ryhmä imukudossyöpiä, joista diffuusi suurisoluinen B-solulymfooma (DLBCL) on yleisin alatyyppi. Se on aggressiivinen maligniteetti, jonka insidenssi on noussut viime vuosina. DLBCL potilaiden ennuste on parantunut merkittävästi, mutta yhä osa potilaista menehtyy tautiinsa. DLBCL:n keskushermostorelapsin kliininen merkitys on tänä päivänä aiempaa suurempi. Sekundaarisen keskushermostolymfooman (sCNSL) ja primaarin aivolymfooman (PCNSL) ennusteet ovat nykyhoidoilla huonoja, joten keskushermostorelapsin ennaltaehkäiseminen on tärkeää. Perifeeriset T-solulymfoomat (PTCLs) ovat ryhmä harvinaisia neoplasioita, joka sisältää useita eri alatyyppejä, joiden morfologiset ja immunofenotyyppiset ominaisuudet ovat monimuotoisia ja osin päällekkäisiä. Eri entiteettien indentifiointi on parantunut, mutta PTCL:ien biologinen tietämys on yhä DLBCL:aa heikompaa. PTCL:ien optimaalinen hoito ei ole selvillä ja tätä tautiryhmää on pitkään hoidettu samoilla hoidoilla kuin DLBCL:aa, mutta huonommilla hoitotuloksilla. Tutkimuksen tavoitteena oli löytää huonon ennusteen markkereita, joilla myös pystyttäisiin ennustamaan DLBCL:n keskushermostorelapsia. Aineisto koostui DLBCL, sCNSL, PCNSL ja PTCL näytteistä. Immunohistokemiallisilla värjäyksillä tutkittiin epiteliaalis-mesenkymaalisen transition (EMT) transkriptiotekijöitä (TF), kemokiinireseptoreita sekä adheesioon-, migraatioon ja inflammaatioon assosioituja molekyylejä. Immunoelektronimikroskopialla varmennettiin molekyylien lokalisaatio soluissa. Geeniekspressioprofiloinnilla (GEP) verrattiin kahdentoista hyvän ja huonon ennusteen ryhmään kuuluvan PTCL näytteen välisiä geeniekspressioeroja sekä kahden DLBCL potilaan näytteitä, joista toiselle kehittyi keskushermostorelapsi. EMT TF:ien ekspressiota nähtiin DLBCL ja PTCL näytteissä, joissa niillä myös todettiin olevan ennusteellista merkitystä. PTCL:ssa TF:t pystyivät erottelemaan tautiryhmän, jolla oli oma spesifinen geeniekspressioprofiilinsa. CXCR4, CXCR5, ITGA10, PTEN ja CD44 ekspressio oli erilaista systeemisissä DLBCL tapauksissa verrattuna sCNSL tapauksiin. Edellä mainituilla molekyyleillä näyttää olevan oma roolinsa keskushermostotaudin kehittymisessä ja jos nämä tulokset pystytään vahvistamaan tulevissa tutkimuksissa, johtavat ne toivottavasti kohti keskushermostorelapsiriskin tarkempaa tunnistamista
Teng, Kun-Yu Teng. "Molecular mechanisms underlying microRNA-122 mediated suppression of liver inflammation, fibrosis, and carcinogenesis." The Ohio State University, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=osu1511206344798557.
Повний текст джерелаWhite, Gemma. "The role of fractalkine (CX₃CL1) and its receptor (CX₃CR1) in vascular biology." Thesis, University of Oxford, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.670108.
Повний текст джерелаCunningham, Crystal. "Expression of Chemokines and VEGFs in HNSCC." VCU Scholars Compass, 2009. http://scholarscompass.vcu.edu/etd/1787.
Повний текст джерелаMadela-Mönchinger, Julia Cecilia. "The impact of rat cytomegalovirus gamma chemokine on dendritic cells." Doctoral thesis, Humboldt-Universität zu Berlin, 2021. http://dx.doi.org/10.18452/22863.
Повний текст джерелаTo date, the two Rat Cytomegalovirus (RCMV) isolates RCMV-England (RCMV-E) and RCMV-Berlin (RCMV-B) are the only known viruses that encode a homolog of XCL1, a gamma- chemokine adopted by viral piracy to interfere with the host’s chemokine network. Like its host homolog, vXCL1 exclusively attracts dendritic cells (DC) that express the XC chemokine receptor 1 (XCR1). In this work, it was investigated whether RCMV misuses the XCL1-XCR1 axis to infect DC in order to disseminate within the host. Initially, rat DC phenotyping revealed two major DC populations, XCR1+ CD4- DC and XCR1- CD4+. It could be shown that supernatants of RCMV-infected rat embryonic fibroblasts solely attracted the XCR1+ CD4- population. Moreover, RCMV was able to infect and replicate in DC. Due to digestion of the spleen and leukocyte enrichment DC became activated leading to full maturation 24 h after cell isolation. During infection, RCMV inhibited the upregulation of several maturation markers including CD40, CD86 and CCR7 and also led to reduced expression of MHCII, CD4 and XCR1. Regardless of vXCL1, RCMV appears to paralyze DC functionality by downregulating maturation genes. In order to analyze the role of XCR1 and vXCL1 function in vivo, Xcr1+/+ and Xcr1-/- rats were infected with RCMV-B wt and RCMV-B delta-vxcl1. Whereas the XCR1 expression level had an influence on the pace of RCMV-B wt dissemination to the salivary glands, the absence of vXCL1 led to a strong decrease in viral spread. DC migration to the salivary glands was dependent on vXCL1 as well as XCR1 and was markedly reduced when vXCL1 and XCR1 were not present. During infection, CD8+ T cells were recruited to the salivary glands, however, this migration was missing when Xcr1+/+ rats were infected with RCMV-B delta-vxcl1. In conclusion, RCMV has the ability to infect DC regardless of vXCL1 expression. RCMV uses vXCL1 to attract XCR1+ DC which appears to be important for viral dissemination to the salivary glands.
Ma, Manhong. "Chemokines and inflammation in wound healing following spinal cord contusion injury in the mouse /." The Ohio State University, 2002. http://rave.ohiolink.edu/etdc/view?acc_num=osu1486462067843737.
Повний текст джерелаPerpiñá, Viciano Cristina [Verfasser], Carsten [Gutachter] Hoffmann, Martin J. [Gutachter] Lohse, and Elke [Gutachter] Butt-Dörje. "Study of the activation mechanisms of the CXC chemokine receptor 4 (CXCR4) and the atypical chemokine receptor 3 (ACKR3) / Cristina Perpiñá Viciano ; Gutachter: Carsten Hoffmann, Martin J. Lohse, Elke Butt-Dörje." Würzburg : Universität Würzburg, 2020. http://d-nb.info/1222910365/34.
Повний текст джерелаLaufer, Julia [Verfasser]. "Characterization of distinct chemokine receptor CCR7 signaling pathways : in health and disease / Julia Laufer." Konstanz : KOPS Universität Konstanz, 2018. http://d-nb.info/1206538953/34.
Повний текст джерелаZhou, Xuefei [Verfasser]. "Funktionelle Charakterisierung des C-Klasse Chemokins ATAC in vivo / Xuefei Zhou." Berlin : Freie Universität Berlin, 2010. http://d-nb.info/1024103714/34.
Повний текст джерелаSmit, Flora [Verfasser]. "Cutaneous defense against Candida albicans: modulation of chemokine-driven anti-microbial immune responses / Flora Smit." Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2018. http://d-nb.info/1172500274/34.
Повний текст джерелаMora, Ahmed. "Expression and function of the chemokine receptor XCR1 on murine CD8 + DC." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2010. http://dx.doi.org/10.18452/16088.
Повний текст джерелаThe G protein-coupled receptor XCR1 has been described as the sole receptor for the chemokine ATAC. As contradictory data were published on the expression pattern of XCR1, its role in the immune system has not yet been defined. In this work, expression of XCR1 was characterized in B6.XCR1 lacZ+/+ reporter mice which express β galactosidase under the control of the XCR1 promoter. In tissue sections, strong expression of XCR1 was only detected in lymphoid organs like spleen, lymph nodes and thymus. In the spleen, XCR1+ cells were mainly found in the marginal zones, but also in the red pulp and the T cell zones. Flow cytometric analysis demonstrated exclusive expression of XCR1 on DC, mainly on the CD8+ DC subset, but also on a minority of CD4− CD8− DC. In vivo, these XCR1+ cells migrated in response to chemotactic or inflammatory stimuli: application of either an ATAC-expressing cell line or LPS induced within 3 9 h the translocation of XCR1+ cells to the T cell area of the spleen. When tested for phagocytic capacity, XCR1+ CD8+ DC, but not other DC subsets, specifically took up injected allogeneic cells, and transfection of these cells with ATAC significantly enhanced their endocytosis by XCR1+ CD8+ DC. Thus, we could employ allogeneic cells expressing OVA intracellularly to target antigen selectively to XCR1+ DC. This antigen targeting induced a strong antigen-specific cytotoxic response by endogenous T cells without a generation of OVA-specific antibodies. In the absence of ATAC, the endogenous cytotoxic activity was markedly diminished. Adoptive transfer and activation of wild type or ATAC-deficient OVA-specific CD8+ transgenic T cells confirmed that ATAC is required for the generation of an optimal cytotoxic response. Targeting of antigen to CD8+ DC via XCR1 may thus be a promising strategy for the development of new vaccination approaches aimed at optimizing the induction of cytotoxic T cells.
Dau, Thérèse Thuy Dung. "Proteolytic modification of elastase and chemokine activities by neutrophil elastase and proteinase 3." Diss., Ludwig-Maximilians-Universität München, 2014. http://nbn-resolving.de/urn:nbn:de:bvb:19-185772.
Повний текст джерелаLachance, Claude. "Role of Fragile X-related protein 1 in controlling the expression of TNF and other pro-inflammatory cytokines and chemokines." Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=32400.
Повний текст джерелаLe facteur onconécrosant de tumeur (TNF) est une cytokine inflammatoire qui joue un rôle important pour combattre diverses infections. La dérégulation de TNF peut cependant entraîner une inflammation non-contrôlée qui est à l'origine de diverses conditions pathologiques. L'expression de TNF est donc fortement régulé aux niveaux transcriptionnels et post-transcriptionnels. Les AREs (éléments riches en adénine\uridine) qui sont présents dans la région 3' non-traduite de l'ARNm de TNF sont reconnus pour leur capacité à stimuler rapidement la dégradation de ces ARNm. Plusieurs protéines se liant aux AREs ont la capacité de médier ce processus. Nous avons identifié une nouvelle protéine, FXR1P (Fragile X-related protein 1) capable de se lier à l'ARE de l'ARNm de TNF. L'utilisation d'une lignée cellulaire de type macrophage provenant de souris où le gène Fxr1 est inactivé a résulté en une expression plus élevée de la protéine TNF sans affecter les niveaux d'ARNm ni la stabilité de ceux-ci. L'analyse de polyribosomes a démontré que l'ARNm de TNF est associé de façon préférentielle avec les fractions lourdes des polyribosomes dans les macrophages FXR1-KO. Ceci indique un rôle de répression de la traduction de l'ARNm de TNF pour FXR1P. Nous avons par la suite définie le rôle de FXR1P lors de l'induction de TNF par les ligands de TLR (récepteur ressemblant à Toll) autres que LPS. Les effets de S28463 (TLR7-L) et de CpG (TLR9-L) ont été testé parce qu'ils possèdent des propriétés thérapeutiques potentielles. La stimulation avec S28463 n'a pas entrainé de différence d'expression de TNF entre les macrophages FXR1-KO et FXR1-WT.
Bird-Gordon, Kereen Suzetta. "Prostate Cancer Cells differentally express anti-inflmmatory and pro-inflammatory cytokines and chemokines: implications for prostate cancer immunotherapy." DigitalCommons@Robert W. Woodruff Library, Atlanta University Center, 2007. http://digitalcommons.auctr.edu/dissertations/12.
Повний текст джерелаMadela-Mönchinger, Julia Cecilia [Verfasser]. "The impact of rat cytomegalovirus gamma chemokine on dendritic cells / Julia Cecilia Madela-Mönchinger." Berlin : Humboldt-Universität zu Berlin, 2021. http://d-nb.info/1233986139/34.
Повний текст джерелаSprague, Leslee W. "Dendritic Cell Culture With 2D and 3D Collagen Substrates." Ohio University / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1311616312.
Повний текст джерелаSchweneker, Marc [Verfasser]. "Identification and characterization of two novel proteins interacting with the chemokine- and HIV-1 co-receptor CCR5 / Marc Schweneker." Berlin : Freie Universität Berlin, 2017. http://d-nb.info/114004351X/34.
Повний текст джерелаHussein, Allami Risala [Verfasser]. "Influence of the chemokine CXCL12 on the progression and the signaling in colorectal cancer / Risala Hussein Allami." Mainz : Universitätsbibliothek Mainz, 2013. http://d-nb.info/1037459539/34.
Повний текст джерелаDau, Thérèse Thuy Dung [Verfasser], and Elisabeth [Akademischer Betreuer] Weiß. "Proteolytic modification of elastase and chemokine activities by neutrophil elastase and proteinase 3 / Thérèse Thuy Dung Dau. Betreuer: Elisabeth Weiß." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2014. http://d-nb.info/107545705X/34.
Повний текст джерелаThobe, Megan. "The Ron Receptor Tyrosine Kinase in Prostate Cancer." University of Cincinnati / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1273006729.
Повний текст джерелаAbe, Philipp [Verfasser], Ralf [Gutachter] Stumm, Christoph Gutachter] Kaether, and Sandra [Gutachter] [Blaess. "Einfluss des Chemokins CXCL12 auf die Entwicklung neuronaler Strukturen / Philipp Abe ; Gutachter: Ralf Stumm, Christoph Kaether, Sandra Blaess." Jena : Friedrich-Schiller-Universität Jena, 2016. http://d-nb.info/1177613239/34.
Повний текст джерелаYester, Jessie. "Intra and extracellular functions of sphingosine-1-phosphate in sterile inflammation." VCU Scholars Compass, 2013. http://scholarscompass.vcu.edu/etd/3245.
Повний текст джерелаNatt, Jessica. "Plasmocytes et désordres immunitaires : impacts des chimiokines et de leurs récepteurs sur la biologie des cellules sécrétrices d’anticorps dans le syndrome WHIM et le lupus systémique." Thesis, Université Paris-Saclay (ComUE), 2017. http://www.theses.fr/2017SACLS375.
Повний текст джерелаThe chemokines (CK) and their receptors (CKR) are essential for leukocyte homeostasis. They are also involved in the pathophysiology of several diseases including the WHIM syndrome and systemic lupus erythematosus (SLE).The WHIM syndrome is a rare immunodeficiency characterised by a severe peripheral lympho-neutropenia. It is caused by a gain-of-function of the CKR CXCR4, leading to a defect in desensitization of this receptor and a hyper-responsiveness to its ligand CXCL12. To better understand the pathophysiology of the WHIM syndrome, our laboratory developed the mouse model Cxcr4+/1013 harboring a natural mutation observed in some patients. Despite the lymphopenia, WHIM patients can mount a potent humoral immune response but that is not sustained over time. The maintenance of long-term antibody (Ab) titers is guaranteed by plasma cells (PCs) in the bone marrow (BM). The first part of my thesis was thus dedicated to the analysis of the role of a gain-of-function of Cxcr4 on PC differentiation and migration. The analysis of humoral response of Cxcr4+/1013 mice revealed a defect in the persistence of specific antibody titres in the absence of Cxcr4 desensitization. Furthermore, this was associated with an abnormal accumulation of a population of immature PCs in the BM.The second part of my work aimed to characterize the migratory potential of circulating PCs from SLE patients. SLE is a systemic autoimmune disease which can affect several organs like the skin, the kidneys or the central nervous system. SLE evolves in flare and remission phases and auto-Ab secreted by autoreactive PCs contribute to its pathophysiology and severity. Today, no specific treatment against autoreactive PCs exist. Targeting their migratory capacity to the inflamed tissues could be an alternative strategy. The objective of this project was to identify the migratory potential of SLE PCs. These studies were processed on samples from SLE patients during flare or remission, and on the lupus mouse model, the NZB/W F1 mice. We observed that the expression of different combinations of surface CKR may stratify several groups of SLE patients
Mehalick, Leslie Ann. "Sphingoid bases induce dose-dependent cytotoxicity and cytokine responses in human myeloid dendritic cells." Thesis, University of Iowa, 2013. https://ir.uiowa.edu/etd/2579.
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