Tesi: "Chemokines"

1

Davis, Christopher Nathan. "Mammalian and viral chemokines provide insight into the mechanism of chemokine receptor activation". [Gainesville, Fla.] : University of Florida, 2004. http://purl.fcla.edu/fcla/etd/UFE0006481.

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2

Hua, Renyi. "The role of chemokines/chemokine receptors in labour". Thesis, Imperial College London, 2012. http://hdl.handle.net/10044/1/9847.

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Human labour is shown to be an inflammatory process, which involves a marked leukocyte infiltrate into myometrium during labour. My study focused on the role of chemokines, key mediators of leukocyte trafficking, in labour. Previous gene array data obtained from human labouring myometrium showed that the mRNA expression of the following chemokines was increased in term labouring myometrium, CCL2, CCL20, CXCL1, CXCL5, CXCL8. I decided to focus on myometrial expression of these chemokines and also to include CCL5, another important chemokine. My data confirmed that the expression of human myometrial chemokines was increased in labour and that their expression was up regulated by cytokines and mechanical stretch via NFKB and MAPK, but decreased by prostaglandins and oxytocin via PLC. I also studied the expression of myometrial chemokine receptors, which may mediate some of the effects of chemokines on myometrial function and/or act as decoys, minimising the effects of locally produced chemokines. I found that the expression of the chemokine receptors decreased with the onset of labour, mainly through the action of prostaglandins and oxytocin. I then used the established model of LPS-‐induced preterm labour (PTL) in the mouse and found that chemokines and cytokines both increased in the myometrium and placenta. CCL2 is consistently increased with human labour and has been shown to be important in rodent parturition too. I therefore studied the impact of LPS in the CCR2 (the main receptor for CCL2) knockout mouse. There was less inflammation in both the myometrium and placenta and a better pup survival rate in the CCR2-/- mouse. However, the PTL was not delayed, suggesting that CCR2 is not essential for the induction of PTL labour by LPS in the mouse. I then turned my attention to CCL20, which acts only via CCR6. It is known to drive dendritic cell recruitment and I found that its expression was increased with labour, while that of its receptor was reduced. Functionally, I found that CCL20 up-regulated the myometrial expression of chemokines. Next I used the LPS-induced preterm labour model in the mouse and found that CCR6 knockout delayed LPS-induced preterm delivery and improved pup survival. These findings were associated with much lower inflammation in myometrium and plasma. These data suggest that CCR6 could be a therapeutic target in the management of PTL. Chemokines play an important role both in the induction of term labour and in infection induced PTL. Chemokine inhibitors may delay the onset of PTL and improve the fetal outcome.

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3

Wong, Jeffrey K. W. "Chemokines and chemokine receptors in islet xenograft rejection". Thesis, The University of Sydney, 2006. https://hdl.handle.net/2123/28055.

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This project investigates the role of chemokine and chemokine receptors in a model of CD4 T cell dependent cellular xenograft rejection, specifically the transplantation of fetal pig pancreas tissue to the renal subcapsular space of mice. Chemokines and chemokine receptor gene expression was assessed by cDNA arrays, and confirmed by multi-probe ribonuclease protection assay. Immunostaining for a selected chemokine, RANTES was performed to demonstrate upregulation at the protein level. These methods were applied to several different models to dissect the role Chemokines and their receptors in this process. Comparisons were made with: an allografi model, a model where indefinite xenograft survival could be achieved by short term costimulatory blockade with CTLA4-Fc and MR1, and an immunodeficient mouse recipient (RAG—1 KO, lacks B and T cells) that was reconstituted with either unfractionated leucocytes or purified CD4 T cells. The main findings were: 1. Allograft rejection and cellular xenografi rejection are THl type CD4 T cell dependent processes as shown by the common T cell chemokine genes (Ltn, IP-lO, and Mig) expressed in both models; however macrophages are the main effector cell in cellular xenografi rejection as evidenced by the selective upregulation of MCP-l and its receptor CCR2, as well as other macrophage markers 2. Of the Chemokines / receptors upregulated in this model of cellular xenograft rejection (Ltn, IP-lO, MCP-l, RANTES, MIP-lB, eotaxin) only MCP-l and IP-lO are CD4 T cell dependent, while Ltn expression is dependent upon a non-CD4 T cell leucocyte subset. 3. CTLA4-Fc and MR1 therapy resulted in indefinite fetal porcine islet survival and function in diabetic immune competent wild type C57BL/6 mice. This treatment suppresses the early upregulation of chemokines and chemokine receptors seen in untreated animals, and this corresponds with a significant reduction CD4 T cell and macrophage grafi infiltration at these time points, consistent with a role for select chemokine / receptors in the mechanism by which this therapy leads to indefinite graft survival. 4. In addition we studied the functioning of fetal porcine islet tissue in diabetic mice and found they developed and controlled glucose metabolism in a piglike manner, and different to normal mice, and thus conclude the development and function of fetal tissue in cross species transplantation is dependent upon the origins of the progenitor cells and not the xenogeneic environment i.e. nature not nurture (in this case anyway). We conclude that select chemokines and their receptors are important factors in the recruitment of effector cells mediating graft rejection in this model of cellular xenograft rejection and these chemokine pathways and networks may represent potential future therapeutic targets.

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4

Mowafi, Frida. "Chemokines and chemokine receptors during viral infections in man /". Stockholm : Karolinska institutet, 2007. http://diss.kib.ki.se/2007/978-91-7357-420-4/.

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5

Teleshova, Natalia. "Studies on co-stimulatory molecules, chemokines and chemokine receptors in neuroimmunological diseases /". Stockholm, 2001. http://diss.kib.ki.se/2001/91-628-4781-3/.

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6

Wang, Jixin. "Bioinformatic analysis of chicken chemokines, chemokine receptors, and Toll-like receptor 21". Texas A&M University, 2006. http://hdl.handle.net/1969.1/4212.

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Chemokines triggered by Toll-like receptors (TLRs) are small chemoattractant proteins, which mainly regulate leukocyte trafficking in inflammatory reactions via interaction with G protein-coupled receptors. Forty-two chemokines and 19 cognate receptors have been found in the human genome. Prior to this study, only 11 chicken chemokines and 7 receptors had been reported. The objectives of this study were to identify systematically chicken chemokines and their cognate receptor genes in the chicken genome and to annotate these genes and ligand-receptor binding by a comparative genomics approach. Twenty-three chemokine and 14 chemokine receptor genes were identified in the chicken genome. The number of coding exons in these genes and the syntenies are highly conserved between human, mouse, and chicken although the amino acid sequence homologies are generally low between mammalian and chicken chemokines. Chicken genes were named with the systematic nomenclature used in humans and mice based on phylogeny, synteny, and sequence homology. The independent nomenclature of chicken chemokines and chemokine receptors suggests that the chicken may have ligand-receptor pairings similar to mammals. The TLR family represents evolutionarily conserved components of the patternrecognizing receptors (PRRs) of the innate immune system that recognize specific pathogen-associated molecular patterns (PAMPs) through their ectodomains (ECDs). TLR's ECDs contain 19 to 25 tandem copies of leucine-rich repeat (LRR) motifs. TLRs play important roles in the activation of pro-inflammatory cytokines, chemokines and modulation of antigen-specific adaptive immune responses. To date, nine TLRs have been reported in chicken, along with a non-functional TLR8. Two non-mammalian TLRs, TLR21 and TLR22, have been identified in pufferfish and zebrafish. The objectives of this study were to determine if there is the existence of chicken genes homologous to fish-specific TLRs, and if possible ligands of these receptors exist. After searching the chicken genome sequence and EST database, a novel chicken TLR homologous to fish TLR21 was identified. Phylogenetic analysis indicated that the identified chicken TLR is the orthologue of TLR21 in fish. Bioinformatic analysis of potential PAMP binding sites within LRR insertions showed that CpG DNA is the putative ligand of this receptor.

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7

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.

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8

Brozyna, Sheree. "The role of chemokines and chemokine receptors in chronic obstructive pulmonary disease (COPD) /". Title page and abstract only, 2005. http://web4.library.adelaide.edu.au/theses/09SB/09sbb8859.pdf.

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9

Simmons, Graham. "Human immunodeficiency syndrome virus type 1 cell tropism and inhibition by chemokines and chemokine analogues". Thesis, Institute of Cancer Research (University Of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.368041.

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10

Juremalm, Mikael. "The Role of Chemokines in Mast Cell Migration". Doctoral thesis, Uppsala University, Department of Genetics and Pathology, 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3273.

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Mast cells are very potent multifunctional effector cells of the immune system normally distributed throughout connective tissues. An accumulation of mast cells has been described in several pathological conditions such as allergic- and autoimmune inflammations and in certain tumours. This necessitates two different processes: 1) Recruitment of mast cell progenitors from peripheral blood; 2) Accretion of mature mast cells at sites of inflammation and tumour areas. Both processes are depending on the local production of chemotactic factors. The aim of this study was to investigate the role of chemokines and their corresponding receptors in mast cell chemotaxis.

By cloning and mRNA-screening of cord blood derived mast cells several chemokine receptors were found to be expressed. Functional expression was confirmed of chemokine receptors CXCR4, CCR1 and CCR4. CXCL12, the only known ligand for CXCR4, acted as a mast cell chemotaxin and induced migration of progenitor cells with capacity to differentiate into mast cells. Of several ligands known to bind CCR1 and CCR4, only CCL5 induced migration of mast cells. The migration to CCL5 was mediated through both CCR1 and CCR4. In contrast, the ligands to CCR4, CCL17 and CCL22, could inhibit CCL5-induced migration. Expression of CCR1 and CCR4 could also be confirmed on mast cells in lung from asthmatic patients. Furthermore, we could demonstrate that mast cells were attracted by CCL5 produced by tumour cells in Hodgkin´s lymphoma.

In conclusion, the work in this thesis has identified two chemokines that regulates mast cell migration. This knowledge helps us understand the mechanisms behind homing of mast cell progenitors from the blood into the tissue and the accumulation of mature mast cells at sites of inflammation and tumourigenesis.

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11

Thapa, Manoj. "Chemokines and chemokine receptors that mediate immune defense to genital herpes simplex virus type 2 (HSV-2) infection". Oklahoma City : [s.n.], 2008.

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12

Hughes, Simon Michael. "Molecular characterisation of avian chemokines". Thesis, University of Reading, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.394177.

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13

Lusti-Narasimhan, Manjula. "The molecular specificity of chemokines". Thesis, University of York, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.362019.

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14

Domingues, Catarina de Barros Pinto Salvador. "Chemokines impact in Alzheimer’s disease". Master's thesis, Universidade de Aveiro, 2015. http://hdl.handle.net/10773/16081.

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Mestrado em Biomedicina Molecular
Alzheimer’s Disease (AD) is a neurodegenerative disorder neuropathologically characterized by the presence of extracellular senile plaques, intracellular neurofibrillary tangles and synaptic loss. Neuroinflammation has been associated with some neurodegenerative diseases, such as AD. In AD, increased Aβ production and aggregation, have a fundamental role in the activation of the inflammatory process. In turn, this could be fundamental in the early stages of this pathology, regarding the Aβ clearance and brain protection. However, chronic inflammation leads to an increase of the inflammatory mediators, such as cytokines, released by activated microglia, astrocytes, and neurons. The excessive production of these inflammatory components promotes alterations in both amyloid precursor protein (APP) expression and processing, stimulating the increase of Aβ accumulation and abnormal tau phosphorylation. This results in neurotoxic effects, irreversible damage and neuronal loss. Chronic inflammation is a feature of AD however, little is known about the effects of some chemokines on its pathogenesis. Thus, the main aim of this thesis was to study the impact of the interleukin-8 (IL-8) and monocyte chemoattractant protein-1 (MCP-1) on apoptosis, APP and tau. The both studied chemokines resulted in small alterations regarding the cytotoxicity on SH-SY5Y differentiated cells, being a significant increase in apoptosis observed only for the MCP-1 at the highest concentration. For the APP processing no significant differences were obtained, although a tendency to increase at different concentrations and periods was registered for both IL-8 and MCP-1. With respect to tau and other cytoskeleton-associated proteins, it was possible to observe a tendency to increase in the phosphorylated residue (Ser396) at the higher concentrations, as well as alterations on actin and tubulin with an increase on acetylated-α tubulin. This effect can be translated by neuronal architectural and survival alterations. Therefore additional studies could contribute to a better understanding of the way that these chemokines act on AD pathogenesis.
A Doença de Alzheimer (DA) é uma doença neurodegenerativa, caracterizada pela presença de placas senis extracelulares, tranças neurofibrilares intracelulares e perda sináptica. A neuroinflamação tem sido associada com algumas doenças neurodegenerativas, tal como a DA. Na DA, a produção e agregação aumentada do péptido Aβ, tem um papel fundamental na activação do processo inflamatório, que pode ser importante nas fases iniciais da doença, devido à remoção de Aβ e à proteção do cérebro. No entanto, uma inflamação crónica leva a um aumento de mediadores inflamatórios como são as citocinas, libertadas por microglia activada, astrócitos e neurónios. A produção excessiva de componentes inflamatórios promove alterações tanto na expressão como no processamento da proteína percursora amilóide (APP), levando a uma maior acumulação de Aβ e fosforilação anormal da proteína tau. Isto resulta em efeitos neurotóxicos, dano irreversível e perda neuronal. A inflamação crónica é uma característica da DA, no entanto pouco se sabe sobre os efeitos de algumas quimiocinas na sua patogénese. Assim, o principal objectivo desta tese foi o estudo do impacto da IL-8 e da MCP-1 na apoptose, APP e tau. Ambas as quimiocinas em estudo resultaram em pequenas alterações ao nível da citotoxicidade de células SH-SY5Y diferenciadas, tendo sido apenas observado um aumento significativo da apoptose para MCP-1 à concentração mais elevada. Relativamente ao processamento de APP, não foram observadas alterações significativas, no entanto alguma tendência para aumentar a diferentes concentrações e períodos foi obtida tanto para a IL-8 como para a MCP-1. Ao nível da tau e outras proteínas associadas ao citoesqueleto, foi possível observar uma tendência de aumento do resíduo fosforilado Ser396 às concentrações mais elevadas assim como alterações na actina e tubulina, com um aumento da αtubulina acetilada. Este efeito pode ser traduzido em alterações na arquitetura e sobrevivência neuronal. Assim sendo, estudos adicionais podem contribuir para uma melhor compreensão do modo de ação destas quimiocinas na patogénese da DA.

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15

Khan, Nouman Ullah. "The effect of chemokines on T regulatory cells following heart transplantation". Thesis, University of Manchester, 2011. https://www.research.manchester.ac.uk/portal/en/theses/the-effect-of-chemokines-on-t-regulatory-cellsfollowing-heart-transplantation(6b5b194d-f2fd-4869-9b22-95ce099ac3ed).html.

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Heart transplantation (HTx) is now an established therapy for end-stage cardiac failure not responding to medical treatment. Recent decades have seen improved outcome following HTx due to more effective and targeted immunosuppressive therapy. However, acute and chronic rejection remains a major cause of morbidity and mortality. At the same time, immunosuppressive strategies are associated with significant side effects, including development of tumours. Hence, the induction of immunologic tolerance to alloantigen is considered the “holy grail” of transplant research. T regulatory cells (Tregs) are a subset of T cells that appear to suppresscytotoxic cell and initiate tolerance to foreign tissues. The Tregs suppresscytotoxic cells through specific cytokine pathways and cell-cell contact. In-vivo T reg migration has been a matter of debate in recent years. Treg trafficking is governed by chemokines, which are small secreted proteins, acting via their distinct trans-membrane serpentine receptors. Experimental work has demonstrated an involvement of distinct chemokine pathways in Tregs migration and localization following cardiac transplantation; however, there is paucity of data in humans. I investigated the effects of chemokines on Tregs in heart transplant recipients through a series of observational studies. My study demonstrated that acute rejection following heart transplantation is associated with a significant elevation of peripheral blood Th1 chemokine levels. I hereby further show that peripheral blood Treg counts in stable heart transplant recipients are not affected by immunosuppression but are significantly lower in patients taking statins. I have demonstrated via in-vitro chemotaxis assays a specific pattern of chemotactic response for Tregs and the effector T cells. Using double immunofluorescence staining and immunostaining, I show for the first time that Tregs may migrate to the allograft under the influence of CCL17.

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16

Kanazawa, Nobuo. "Fractalkine and macrophage-derived chemokine : T cell attracting chemokines expressed in T cell area dendritic cells". Kyoto University, 2000. http://hdl.handle.net/2433/180886.

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17

Negus, R. P. M. "Chemokines, leukocytes and human ovarian cancer". Thesis, Imperial College London, 1998. http://hdl.handle.net/10044/1/7211.

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18

McQuibban, Angus. "Matrix metalloproteinase processing of monocyte chemokines". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/NQ61145.pdf.

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19

Uddin, Jasim. "Chemokines and inflammatory responses in cysticercosis". Thesis, Imperial College London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.407076.

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20

Kuschert, Gabriele Simone Viktoria. "Chemokines and their interaction with glycosaminoglycans". Thesis, University of York, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.298530.

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21

Franciszkiewicz, Katarzyna. "The role of chemokines and chemokine receptors in shaping the effector phase of anti-tumor immune response". Paris 7, 2010. http://www.theses.fr/2010PA077015.

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La réponse immunitaire antitumorale nécessite la mise en place de mécanismes effecteurs dépendant des lymphocytes T CD8+ cytotoxiques spécifiques. Cependant, leur présence n'est pas toujours suffisante pour induire une régression tumorale dépendant de plusieurs étapes: la migration des lymphocytes T au site tumoral, l'infiltration, l'établissement de contacts avec le cible cancéreuse et l'activation in situ. Les chimiokines sont impliquées dans la circulation des cellules immunocompétentes. Bien que leur rôle dans la progression tumorale soient bien établi, les chimiokines sont également responsable de la modulation du microenvironnement tumoral permettant l'infiltration des lymphocytes et la potentialisation de leurs fonctions effectrices. Nous avons démontré que les effecteurs T cytotoxiques peuvent être recrutés par la tumeur autologue de façon dépendante du récepteur aux chimiokines CCR5. Une fois dans microenvironnement tumorale riche en TGF-β, ils subissent un processus d'adaptation résultant en l'induction de l'expression du récepteur aux chimiokines CCR6 et de l'intégrine aEβ7, ainsi qu'en la potentialisation de leur activité cytotoxique. L'engagement de l'intégrine aEβ7 conduit au recrutement de CCR5 dans la synapse immunologique, provoquant ainsi la désensibilisation des lymphocytes T au gradient de CCL5. Nos travaux ont mis en évidence le rôle majeur des chimiokines dans le développement de la réponse immunitaire antitumorale dépendante de lymphocytes T cytotoxiques. Dans cette optique, l'identification des mécanismes moléculaires induits par les chimiokines correspond à un enjeu important pour l'optimisation des protocoles d'immunothérapie antitumorale
The immune system-mediated eradication of cancer cells requires effector mechanisms associated with the presence of tumor-specific T cells. However, the successful generation of tumor-specific effector cells does not necessarily result in tumor regression. Cytotoxic T lymphocytes (CTL) must first be able to migrate to tumor sites, traverse the interstitial space and fmally interact with their target resulting in triggering of effector fonctions. Chemokines are involved in circulation of immunocompetent cells. Although some of them are known to contribute to tumor progression, others are responsible for changes in the tumor microenvironment that allow the infiltration of lymphocytes. In this study, we demonstrate that CTLs can be efficiently recruited into the tumor in a CCR5-dépendent manner. Once in the TGF-pl-rich autologous tumor site, they undergo an intratumoral adaptation process resulting in upregulation of the chemokine receptor CCR6 and the integrin aEß7 as well as the enhancement of T-cell receptor (TCR)-mediated cytotoxicity. The engagement of aEβ₇ leads to CCR5 recruitment at the IS and reduced T-cell responsiveness to a CCR5 ligand chemotactic gradient, suggesting a role of aEß7 in T-cell rétention at the tumor by a CCR5-dépendent mechanism. Altogether, these results show an important role of the chemokine/chemokine receptor network at multiple levels of CTL-mediated antitumor immune response. In consequence, the identification of chemokine-medjated molecular mechanisms can be important for the development of innovative immunotherapeutic approaches and may offer new opportunities to optimize existing protocols of cancer therapy

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22

Law, Yuet Ching. "Specific Compartmentalization of IgA ASCs in Mouse Salivary Glands via Differential Expression of Chemokines and Chemokine Receptors". BYU ScholarsArchive, 2008. https://scholarsarchive.byu.edu/etd/1952.

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The mucosal system, which forms a barrier between internal organ systems and the external environment, is frequently exposed to pathogenic microorganisms. Immunoglobulin A (IgA) antibody secreting cells (ASCs) localize in the lamina propria, and produce IgA antibodies which help protect mucosal tissues. The concept of a common mucosal immune system in which IgA ASCs have the ability to populate any mucosal site has been proposed (1, 2). However, recent research has suggested that IgA ASCs primed in different mucosal sites might possess different sets of chemokine receptors, and therefore migrate specifically to particular mucosal locations (3). In this study, the specific compartmentalization of IgA ASCs in two mouse salivary glands: sublingual gland (SLG), and submandibular gland (SMG) was studied. It was observed that SLG had 12 times more IgA ASCs per gram of gland than that of SMG (p<0.01). This suggested that IgA ASCs migrated to the two salivary glands with different efficiencies. Since the migration of lymphocytes is mediated by interactions between tissue specific chemokines and chemokine receptors, I hypothesized that the specific compartmentalization of IgA ASCs in the SLG and SMG was mediated by the differential expression of IgA ASC attracting chemokines. Quantitative PCR was used and showed that SLG expressed high levels of CCL28 and its receptor CCR10, which correlated to the distribution of IgA ASCs in the two salivary glands. In agreement with QPCR data, reduced levels of IgA ASCs were found in the SLG of CCR10 deficient mice when compared to wild type (WT) mice. Adoptive transfer of CCR10 deficient mice with WT spleen cells reconstituted the WT phenotype. It was therefore concluded that the interaction between CCL28 and CCR10 play an important role in mediating the migration of IgA ASCs into SLG. These results suggested that the accumulation of IgA ASC to distinct salivary glands is a highly selective process. These data also suggested that homing within mucosal sites is not common but rather a highly regulated process with specific subsets of cells homing to different tissues within the mucosal immune system.

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Jin, Hongjun. "Structural and functional investigation of human chemokines and applications of human chemokines in blocking HIV-1 entry". [College Station, Tex. : Texas A&M University, 2007. http://hdl.handle.net/1969.1/ETD-TAMU-2430.

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Law, Yuet Ching. "Specific compartmentalization of Immunoglobulin A antibody secreting cells in mouse salivary glands via the differential expression of chemokines and chemokine receptors /". Diss., CLICK HERE for online access, 2008. http://contentdm.lib.byu.edu/ETD/image/etd2678.pdf.

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Timár, Krisztina Klára. "Human keratinocytes production of complement and chemokines /". [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2006. http://dare.uva.nl/document/20321.

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Scotton, Christopher John. "Chemokines and their receptors in ovarian cancer". Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.395391.

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McNaughton, Emily Francis. "Novel anti-inflammatory peptides based on chemokines". Thesis, University of Bristol, 2017. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.730839.

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28

Cunningham, Crystal. "Expression of Chemokines and VEGFs in HNSCC". VCU Scholars Compass, 2009. http://scholarscompass.vcu.edu/etd/1787.

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Abstract (sommario):

Head and neck squamous cell carcinoma (HNSCC) is the sixth most common malignancy worldwide. The 5-year survival rate when the cancer remains as a primary tumor is 81% but when it metastasizes to distant sites, defined as a metastatic cancer, it decreases dramatically to 26%. Approaches to prevent these cancers from undergoing these metastatic changes can greatly improve the survival and outcome of these cancer victims. This current study is examining the expression profiles of chemokines and VEGFs in HNSCC. By investigation the underlying pathways involved in the expressions of chemokines and VEGFS we hope to sort out the transcriptional regulation of these molecules. We used pharmological inhibitors of several important kinase pathways and the receptors involved in the transcription of chemokines and VEGFs. This study specifically looked at the proangiogenetic chemokines, CXCL5 and CXCL8, and their receptor CXCR2, and their possible impact on VEGFs, specifically VEGF-C and VEGF-A. From experimentation we concluded that HNSCC uses the MAPK pathway for regulation of the chemokines CXCL5 and CXCL8, but not for its downregulation. VEGF-A showed to be positively controlled by the MAPK pathway. The Akt pathway was found to downregulate VEGF-C, possibly from CXCR2. VEGF-C was not under control of the chemokines’ expression, VEGF-C and VEGF-A were also differentially regulated. The current study has begun to sort out the expression and regulation of chemokines and VEGFs in HNSCC. There are still many unanswered questions about the role these molecules play in HNSCC, but hopefully these conclusions will aid in finding improved treatments for patients diagnosed with head and neck cancer.

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Edman, Linda C. "Chemokines and their role in dopaminergic development". Stockholm : Department of Medical Biochemistry and Biophysics, Karolinska Institutet, 2009. http://diss.kib.ki.se/2009/978-91-7409-688-0/.

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30

Ridiandries, Anisyah. "The role of cc-chemokines in angiogenesis". Thesis, The University of Sydney, 2015. http://hdl.handle.net/2123/14951.

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Angiogenesis is a fundamental process in which new blood vessels are formed from pre-existing vessels. It is important in growth, development, and regeneration after injury. Inflammation causes an imbalance in the regulation of angiogenesis leading to unregulated pathological neovascularisation that exacerbates diseases such as cancer and atherosclerosis. Current anti-angiogenic therapies for the treatment of these diseases inhibit both pathological and physiological angiogenesis causing side effects such as hypertension, bleeding, severe weight loss, diarrhoea and nausea in a large percentage of patients. Increasing evidence suggests the CC-chemokine class promote inflammatory-driven angiogenesis, with little-to-no effect in hypoxia-mediated angiogenesis. Inhibition of the CC-chemokine class may therefore regulate angiogenesis differently depending on the pathophysiological context. The main objectives of the present studies were to compare the role of CC-chemokines in both inflammatory-driven and ischaemia-mediated angiogenesis using a broad-spectrum CC-chemokine specific inhibitor "35K". The studies presented in this thesis demonstrate for the first time that broad-spectrum CC-chemokine inhibition by 35K attenuates inflammatory-driven pathological angiogenesis whilst preserving ischaemia-mediated neovascularisation in vitro and in vivo.

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31

宋蘭。 e Lan Fion Sung. "Role of homocysteine in the expression of monocyte Chemoattractant protein-1 (MCP-1)". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1999. http://hub.hku.hk/bib/B31221658.

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Sung, Lan Fion. "Role of homocysteine in the expression of monocyte Chemoattractant protein-1 (MCP-1) /". Hong Kong : University of Hong Kong, 1999. http://sunzi.lib.hku.hk/hkuto/record.jsp?B21038338.

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33

Conrad, Sean Martin. "The influence of parasite-derived chemokines in Leishmaniasis". College Park, Md. : University of Maryland, 2006. http://hdl.handle.net/1903/4247.

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Abstract (sommario):

Thesis (Ph. D.) -- University of Maryland, College Park, 2006.
Thesis research directed by: Cell Biology & Molecular Genetics. Title from t.p. of PDF. Includes bibliographical references. Published by UMI Dissertation Services, Ann Arbor, Mich. Also available in paper.

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34

Poh, Tuang Yeow. "Functional characterization of avian chemokines and their receptors". Thesis, Imperial College London, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.441954.

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35

Darisipudi, Venkata Surya Narayana Murty. "Chemokines and cysteine proteases in diabetic kidney disease". Diss., Ludwig-Maximilians-Universität München, 2013. http://nbn-resolving.de/urn:nbn:de:bvb:19-173379.

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36

Kirkaldy, Alice Amanda. "The role of chemokines in leprosy skin lesions". Thesis, London School of Hygiene and Tropical Medicine (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.268729.

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37

Marshall, Alison Shona. "The role of chemokines in oral lichen planus". Thesis, University College London (University of London), 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.413748.

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38

Lipfert, Jana. "Die Rolle und Funktionsweise der Chemokinrezeptoren CXCR4 und CXCR7 in Mikroglia und Astrozyten". Doctoral thesis, Universitätsbibliothek Leipzig, 2013. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-118858.

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Abstract (sommario):

Das Chemokin SDF-1 spielt eine wichtige Rolle bei der Hämatopoese, bei Immunreaktionen sowie bei der Entwicklung des Herzens, der Extremitätenmuskulatur und des zentralen und peripheren Nervensystems. Lange Zeit galt CXCR4 als der einzige Chemokinrezeptor für SDF-1, bis vor wenigen Jahren CXCR7 als ein alternativer Rezeptor für SDF-1 identifiziert wurde. Da alle Zelltypen des zentralen Nervensystems (ZNS) sensitiv für SDF-1 sind, sollte in dieser Arbeit die Funktion der beiden Rezeptoren in primärer Mikroglia und primären Astrozyten untersucht werden. Bisher konnte CXCR7 nur als Scavenger-Rezeptor für SDF-1 oder als atypischer Chemokinrezeptor nachgewiesen werden. Die Untersuchungen ergaben einen mitogenen und chemotaktischen Effekt von SDF-1 auf primäre Mikroglia, wobei sowohl CXCR4 als auch CXCR7 für das SDF-1-Signalverhalten essentiell sind. Nach Aktivierung von Mikroglia in vitro und in vivo wurden beide Rezeptoren verstärkt expremiert. In primären Astrozyten ergab sich ein ligandenabhängiges Signalverhalten von CXCR7. So führte die Bindung von SDF-1 an CXCR7 zu einer Aktivierung von G-Proteinen, während die Kopplung von interferon-inducible T cell alpha chemoattractant (I-TAC), als zweiten Liganden von CXCR7, eine Signalweiterleitung über ß-Arrestin2 zur Folge hatte. Zudem konnte die G-Protein-gekoppelte Rezeptorkinase (Grk)2 als ein positiver Regulator des SDF-1-CXCR7-Signalverhaltens in Astrozyten identifiziert werden.

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39

Dagkalis, Athanasios. "CCR2 and CX3CR1 in monocyte trafficking in experimental autoimmune uveoretinitis". Thesis, Available from the University of Aberdeen Library and Historic Collections Digital Resources, 2008. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=24809.

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40

Cavalcante, GalylÃia Menezes. "Study of expression of systems CXCR4-CXCL12/SDF-1, CCR7-CCL21 and Ki-67 in the oral squamous cell carcinoma and their association with clinicopathological factors,nodal metastases and survival". Universidade Federal do CearÃ, 2013. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=11989.

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Abstract (sommario):

Chemokines are responsible for the directed migration of leukocyte chemotactic cytokines, coordinating cell movement during inflammation and the transport of hematopoietic cells. In addition to leukocytes, chemokine receptors are also found in neoplastic cells and tumors associated with stromal cells. Among chemokines, and the CXCR4/CXCL12 CCR7/CCL21 systems have been shown the involvement of lymph node metastases or distant metastases in different cancers. Thus, aim of this study was to evaluate the expression of CXCR4, CXCL12, CCR7, CCL21 and Ki-67 in oral squamous cell carcinoma (SCC) and to correlate these markers with clinicopathological indicators, lymph node metastasis and survival. We conducted a survey of reports and paraffin blocks of excisional biopsies of patients with SCC treated at the Hospital Haroldo JuaÃaba (2001-2009). Data on anatomic location of the lesion, sex, age, patient survival, degree of histological differentiation of the tumor, tumor stage and presence or absence of lymph node metastasis, lymphovascular and perineural invasion, nuclear grade and depth of invasion were collected. For immunohistochemical analysis, followed by the technique of streptavidin-biotin-peroxidase using the anti-CXCR4, anti-CXCL12, anti-CCR7, anti-CCL21 and Ki-67 antibody. Histological sections were photomicrographed in 10 fields chosen randomly and measured for the number of labeled tumor cells and determined the percentage of each labeling antibody. The marking of CXCR4 was detected in the cytoplasm and nucleus, CXCL12, CCR7 and CCL21 were only cytoplasmic, their expression was observed in 18 (60%) 8 (22.66%) 16 (53.3%) and 3 (12%) cases, respectively. We found a significant positive association between lymphovascular invasion and immunostaining of CXCR4 (p = 0.007) and CCR7 (P = 0.01) and among these cases metastasis was present in 62.5% and 37.5%, respectively. When in combination with Ki67, we found a significant positive correlation between CXCR4 (p = 0.0086), CXCL12 (p = 0.036) and CCR7 (p = 0:04). Among patients CXCR4 + over 111 months, only 38.4% were alive (p = 0.845), whereas both patients CCR7 + (p = 0.398) as well as CXCR4 +, and CCR7 + (p = 0.441) after 62 months, everyone had already died. We conclude that these chemokines are associated with lymphovascular invasion and cell proliferation, perhaps favoring the development of metastasis and poor prognosis.
As quimiocinas sÃo citocinas quimiotÃticas responsÃveis pela migraÃÃo direcionada de leucÃcitos, coordenando o movimento celular durante a inflamaÃÃo e o transporte de cÃlulas hematopoiÃticas. AlÃm dos leucÃcitos, os receptores de quimiocinas tambÃm sÃo encontrados em cÃlulas neoplÃsicas e em tumores associados com cÃlulas estromais. Dentre as quimiocinas, os sistemas CXCR4/CXCL12 e CCR7/CCL21 tÃm sido demonstrado no envolvimento de metÃstases linfonodais ou Ã distÃncia em diferentes tipos de cÃncer. Dessa forma, foi objetivo desse trabalho avaliar a expressÃo de CXCR4, CXCL12, CCR7, CCL21 e Ki-67 em carcinoma de cÃlulas escamosas orais (CEC) e correlacionar estes marcadores com indicadores clÃnicopatolÃgicos, metÃstase linfonodal e sobrevida. Realizou-se um levantamento de laudos e blocos parafinados de biopsias excisionais de pacientes portadores de CEC tratados no Hospital Haroldo JuaÃaba (2001 a 2009). Foram coletados dados sobre localizaÃÃo anatÃmica da lesÃo, sexo, idade, sobrevida do paciente, grau de diferenciaÃÃo histopatolÃgica do tumor, estadiamento tumoral e presenÃa ou ausÃncia de metÃstase linfonodal, invasÃo linfovascular e perineural, grau nuclear e profundidade de invasÃo. Para reaÃÃo de imunohistoquÃmica, seguiu-se a tÃcnica da estreptavidina-biotina-peroxidase, utilizando os anticorpos anti-CXCR4, anti-CXCL12, anti-CCR7, anti-CCL21 e Ki-67. As secÃÃes histolÃgicas foram fotomicrografadas em 10 campos escolhidos aleatoriamente e quantificadas quanto ao nÃmero de cÃlulas tumorais marcadas e determinado o percentual de marcaÃÃo de cada anticorpo. A marcaÃÃo de CXCR4 foi detectada em citoplasma e nÃcleo, CXCL12, CCR7 e CCL21 tiveram marcaÃÃo apenas citoplasmÃtica, sendo observada suas expressÃes em 18 (60%), 8 (22,66%), 16 (53,3%) e 3 (12%) casos, respectivamente. Encontrou-se uma associaÃÃo significativa positiva entre a invasÃo linfovascular e a imunomarcaÃÃo do CXCR4 (p=0.007) e CCR7 (p=0.01) e dentre esses casos a metÃstase esteve presente em 62,5% e 37,5%, respectivamente. Quando em associaÃÃo com o Ki67, encontrou-se uma correlaÃÃo positiva significante entre o CXCR4 (p=0.0086), CXCL12 (p=0.036) e CCR7 (p=0.04). Dentre os pacientes CXCR4+, ao longo de 111 meses, apenas 38,4% estavam vivos (p=0.845), ao passo que tanto para pacientes CCR7+ (p = 0.398), quanto CXCR4+ e CCR7+ (p = 0.441), apÃs 62 meses, todos haviam ido a Ãbito. Conclui-se que essas quimiocinas estÃo associadas com a invasÃo linfovascular e proliferaÃÃo celular, talvez favorecendo o desenvolvimento de metÃstases e um pior prognÃstico.

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41

Oladipo, O. "The clinical role of cxc-chemokines in colorectal cancer". Thesis, Queen's University Belfast, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.546403.

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42

Montero, Rosa Maria. "Chemokines and macrophage migration inhibitory factor in diabetic nephropathy". Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/29851.

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Introduction: Diabetic nephropathy (DN) is the leading cause of end-stage renal disease in the Western world. Aim: To determine whether macrophage migration inhibitory factor (MIF), monocyte chemoattractant protein-1 (MCP-1) or CC chemokine ligand 18 (CCL18) have a causative role in the development of renal inflammation and fibrosis in DN and are useful biomarkers of disease progression. Methods: Urine and plasma samples were collected from 115 DM and 116 Non-DM at baseline, previously analysed for MCP-1 and CCL18 ELISA by Dr Qureshi. I measured MIF in these samples and collected 107 DM and 114 Non-DM data points (GFR, ACR/UPCR and clinical parameters) at >18 months and >3 years. MIF, MCP-1 and CCL18 urine, plasma and serum analysis was performed in 42 DM and 60 Non-DM at >3 years follow up. Intrinsic renal cells were cultured and stimulated with diabetic conditions. These cytokines and fibronectin were measured in tubuloepithelial cells and podocytes. Results: Baseline plasma CCL18 and MIF predicted a decline in GFR in DM at >18 months but not at >3 years. Cytokine production varies over time with significant correlations at baseline that are not maintained. Cytokines correlate differently with GFR, ACR/UPCR in DM versus Non-DM proteinuric renal diseases. Plasma and serum cytokine levels correlated significantly with no correlation between these and urinary levels. All intrinsic renal cells were able to produce MIF, MCP-1 and CCL18 following stimulation. The interaction of these cytokines and their effects on fibronectin vary in diabetic conditions and following recombinant cytokine stimulation. The diabetic environment appears to orchestrate cytokine signals according to cell type. Conclusion: These results suggest cytokines may play a key role in the pathogenesis and or progression of DN. The clinical study suggests cytokines may predict progression; however, larger studies are needed with samples taken at different time points.

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43

Rosenblum, Joshua Michael. "Novel Roles for Chemokines in Acute Cardiac Allograft Rejection". Case Western Reserve University School of Graduate Studies / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=case1244063137.

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44

Kwong, Amelia. "Crosstalk Between T Cells, Dendritic Cells, Cytokines, and Chemokines". Thesis, The University of Arizona, 2010. http://hdl.handle.net/10150/146198.

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T cells that came into contact with mature and immature dendritic cells had an overall reduction in gene expression in IL10, IL12, IL23, ICOS, TGFB, TNFA, PD1, TBET, GATA3, FASL, PERF, FOXP3, and CTLA4. T cells stimulated with immature dendritic cells had the most consistent results in decreasing gene expression in all the genes tested. T cells in contact with mature dendritic cells had mostly a decrease in gene expression, but in IFNG and Granzyme there was an increase in gene expression. However, when adding additional stimuli such as interferon(IFN) or hydroxychloroquine (HCQ) gene expression increased in all of the markers except for TGFB, PERF, and IL12. This leads me to believe that crosstalk is occurring between dendritic cells and T cells. This crosstalk could direct the particular cells to perform specialized functions, which can explain the increase and decrease of the markers tested. In addition, interferon and hydroxychloroquine seems to hyper-stimulate most markers to create an up regulation of gene expression.

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45

Lin, Michelle. "Facilitation of neutrophil migration through the corneal stroma during keratitis-Mmp8 and chemokines". Connect to text online, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=case1191012168.

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46

Yu, Tian. "Role of atypical chemokine receptor-2 in ocular inflammation". Thesis, University of Aberdeen, 2015. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=229021.

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The atypical chemokine receptor-2 (ACKR2) is a chemokine decoy receptor that recognises pro-inflammatory CC chemokines. Many studies showed up-regulated inflammation and delayed resolution of inflammatory responses in ACKR2-/- mice. Furthermore, in the absence of ACKR2, lymphatic endothelial cells (LEC) fail to regulate the expression of pro-inflammatory CC chemokines leading to the excessive peri-lymphatic accumulation of leukocytes. As a result, the migration of antigen presenting cells (APC) through lymphatic vessels may be impaired due to lymphatic congestion. In addition, ACKR2 was shown to regulate lymphatic vessel density in the embryonic skin by regulating the proximity of pro-lymphangiogenic macrophages to LEC. Therefore, to address the role of ACKR2 and its significance in 1) APC migration and 2) inflammation-associated lymphangiogenesis, three models of ocular inflammation were used in this work, experimental autoimmune uveoretinitis (EAU), corneal graft rejection and herpes simplex keratitis (HSK). With regard to APC migration, in both EAU and HSK models, this process was fine-tuned to the level of disease in that migration was significantly compromised in ACKR2-/- mice during severe inflammation, but not under mild inflammatory conditions. Furthermore, while the severity of EAU was associated with the migration of APC, this was not so in HSK. In order to study lymphangiogenesis, the transparent avascular cornea provides a good substrate and corneal lymphangiogenesis was studied using both corneal graft model and HSK model. I found that lymphatic vessel density was increased in ACKR2-/- mice compared to wild type mice in corneal graft induced lymphangiogenesis (macrophage mediated), but not altered during early stages of HSK associated lymphangiogenesis (non-macrophage mediated). These findings confirmed that ACKR2 indirectly regulates the process of lymphangiogenesis in a macrophage dependent manner. Although the severity of HSK correlated with the level of lymphangiogenesis, this does not seem to correlate with viral load but rather associated with inflammatory infiltrations in the cornea.

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47

Caronni, N. "ROLE OF CCL2 AND ITS RECEPTORS CCR2 AND D6 IN THE ACTIVATION AND POLARIZATION OF TUMOR-ASSOCIATED MACROPHAGES". Doctoral thesis, Università degli Studi di Milano, 2014. http://hdl.handle.net/2434/229564.

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Chemokines are well known to play a major role in tumor progression and metastasis. In particular CCL2 is over-expressed in several human cancers and their higher levels correlate with poor prognosis and shorter outcomes. Here we reported two different studies in which CCL2 receptors, the canonical CCR2 and the atypical D6 (or ACKR2) were examined for their involvement in tumor progression. In particular D6 was investigated for its expression and its ability to shape CCL2 gradient in Kaposi’s sarcoma, whereas CCR2 has been analyzed as potential modeler of TAM polarization. D6 is an atypical chemokine receptor acting as a decoy and scavenger for inflammatory CC chemokines expressed in lymphatic endothelial cells. Here, we report that D6 is also expressed by Kaposi’s sarcoma (KS) which is a tumor ontogenetically related to lymphatic endothelium, yet its role in tumor progression was hitherto unknown. D6 expression was evaluated by immunohistochemistry in a cohort of KS patients and its role in cancer progression was investigated in an in vivo KS model. Both in human tumors and in the experimental model, D6 expression levels were inversely correlated with tumor aggressiveness, and directly correlated with increased chemokine-driven infiltration of macrophages and their acquisition of a pro-angiogenic phenotype. Inhibition of monocyte recruitment reduced growth of D6-incompetent tumors, while adoptive transfer of wt but not CCR2-/- macrophages increased the growth rate of D6-competent neoplasms. In the KS model, which presents the B-Raf V600E activating mutation, inhibition of B-Raf or downstream ERK pathway induced D6 expression, and in progressing human KS tumors activation of the K-Ras/B-Raf/ERK pathway correlate with reduced levels of D6 expression. These results indicate that activation of the K-Ras/B-Raf/ERK pathway during KS progression down-regulates D6 expression, which unleashes chemokine-mediated macrophage recruitment and their acquisition of an M2-like phenotype supporting angiogenesis and tumor growth. Thereafter, we wanted to deeper investigate how CCR2 support TAM M2 polarization firstly by using an in vitro system. Wt and CCR2-/- macrophages were polarized with M1 and M2 stimuli and analyzed for gene expression and cytokines production. While no difference was found in M2 polarized macrophages, CCR2-/- M1 or LPS activated macrophages showed higher expression of inflammatory genes and reduced production of the anti-inflammatory cytokine IL-10 and of the pro-angiogenic cytokine VEGF when compared to wt macrophages. The impaired IL-10 production was also confirmed by treating human monocytes with the CCR2 antagonist RS-504393. After LPS stimulation, CCR2-/- macrophages showed reduced activation of NF-kB and p38 MAPK when compared to wt macrophages indicating a cross talk between CCR2 and TLR4 signaling pathways. The contribution of CCR2 to cancer growth was evaluated with a transplantable lung cancer model that grew slower when co-injected with CCR2-/- macrophages, presenting a marked M1 phenotype of infiltrating TAM and a higher number of both CD4+ and CD8+ T cells, correlated with a decreased number of splenic T regulatory cells when compared to wt macrophages holding-tumors. Taken together these data indicate that CCR2 expression by macrophages not only induce their recruitment to tumor site but also affect their polarization and anti-tumor potential.

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48

Sayyed, Sufyan G. "Role of pro-inflammatory and homeostatic chemokines in diabetic nephropathy". Diss., lmu, 2010. http://d-nb.info/1001123050/34.

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49

Bradford, Eric, Sean Jacobson, Jason Varasteh, Alejandro P. Comellas, Prescott Woodruff, Wanda O’Neal, Dawn L. DeMeo et al. "The value of blood cytokines and chemokines in assessing COPD". BIOMED CENTRAL LTD, 2017. http://hdl.handle.net/10150/626086.

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Background: Blood biomarkers are increasingly used to stratify high risk chronic obstructive pulmonary disease (COPD) patients; however, there are fewer studies that have investigated multiple biomarkers and replicated in multiple large well-characterized cohorts of susceptible current and former smokers. Methods: We used two MSD multiplex panels to measure 9 cytokines and chemokines in 2123 subjects from COPDGene and 1117 subjects from SPIROMICS. These biomarkers included: interleukin (IL)-2, IL-6, IL-8, IL-10, tumor necrosis factor (TNF)-alpha, interferon (IFN)-gamma, eotaxin/CCL-11, eotaxin-3/CCL-26, and thymus and activation-regulated chemokine (TARC)/CCL-17. Regression models adjusted for clinical covariates were used to determine which biomarkers were associated with the following COPD phenotypes: airflow obstruction (forced expiratory flow at 1 s (FEV1%) and FEV1/forced vital capacity (FEV1/FVC), chronic bronchitis, COPD exacerbations, and emphysema. Biomarker-genotype associations were assessed by genome-wide association of single nucleotide polymorphisms (SNPs). Results: Eotaxin and IL-6 were strongly associated with airflow obstruction and accounted for 3-5% of the measurement variance on top of clinical variables. IL-6 was associated with progressive airflow obstruction over 5 years and both IL-6 and IL-8 were associated with progressive emphysema over 5 years. None of the biomarkers were consistently associated with chronic bronchitis or COPD exacerbations. We identified one novel SNP (rs9302690 SNP) that was associated with CCL17 plasma measurements. Conclusion: When assessing smoking related pulmonary disease, biomarkers of inflammation such as IL-2, IL-6, IL-8, and eotaxin may add additional modest predictive value on top of clinical variables alone.

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50

Ramwell, Andrew P. "The Role of Chemokines and their Receptors in Colorectal Cancer". Thesis, Imperial College London, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.511887.

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