Academic literature on the topic 'Atypical Chemokine Receptors'
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Journal articles on the topic "Atypical Chemokine Receptors"
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Hansell, C. A. H., C. V. Simpson, and R. J. B. Nibbs. "Chemokine sequestration by atypical chemokine receptors." Biochemical Society Transactions 34, no. 6 (October 25, 2006): 1009–13. http://dx.doi.org/10.1042/bst0341009.
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Leucocyte migration is essential for robust immune and inflammatory responses, and plays a critical role in many human diseases. Chemokines, a family of small secreted protein chemoattractants, are of fundamental importance in this process, directing leucocyte trafficking by signalling through heptahelical G-protein-coupled receptors expressed by the migrating cells. However, several mammalian chemokine receptors, including D6 and CCX-CKR (ChemoCentryx chemokine receptor), do not fit existing models of chemokine receptor function, and do not even appear to signal in response to chemokine binding. Instead, these ‘atypical’ chemokine receptors are biochemically specialized for chemokine sequestration, acting to regulate chemokine bioavailability and thereby influence responses through signalling-competent chemokine receptors. This is of critical importance in vivo, as mice lacking D6 show exaggerated cutaneous inflammatory responses and an increased susceptibility to the development of skin cancer. CCX-CKR, on the other hand, is predicted to modulate homoeostatic lymphocyte and dendritic cell trafficking, key migratory events in acquired immune responses that are directed by CCX-CKR-binding chemokines. Thus studies on ‘atypical’ chemokine receptors are revealing functional and biochemical diversity within the chemokine receptor family and providing insights into novel mechanisms of chemokine regulation.
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Borroni, Elena M., Raffaella Bonecchi, and Annalisa M. VanHook. "Science Signaling Podcast: 30 April 2013." Science Signaling 6, no. 273 (April 30, 2013): pc11. http://dx.doi.org/10.1126/scisignal.2004231.
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This Podcast features an interview with Elena M. Borroni and Raffaella Bonecchi, authors of a Research Article that appears in the 30 April 2013 issue of Science Signaling. Chemokines recruit leukocytes to sites of infection and inflammation by binding to chemokine receptors, which are members of the G protein–coupled receptor superfamily, present on the surface of leukocytes. Whereas activation of typical chemokine receptors leads to G protein–dependent signaling that promotes cell migration toward the chemokine source, activation of atypical chemokine receptors does not promote cell migration. Instead, signaling initiated by atypical chemokine receptors contributes to the immune response in other ways. The atypical chemokine receptor D6 is a scavenger that alters the chemokine gradient by binding to and degrading chemokines. Borroni and Bonecchi found that activation of a β-arrestin–dependent signaling pathway was necessary for D6 to act as a chemokine scavenger.
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Groblewska, Magdalena, Ala Litman-Zawadzka, and Barbara Mroczko. "The Role of Selected Chemokines and Their Receptors in the Development of Gliomas." International Journal of Molecular Sciences 21, no. 10 (May 24, 2020): 3704. http://dx.doi.org/10.3390/ijms21103704.
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Among heterogeneous primary tumors of the central nervous system (CNS), gliomas are the most frequent type, with glioblastoma multiforme (GBM) characterized with the worst prognosis. In their development, certain chemokine/receptor axes play important roles and promote proliferation, survival, metastasis, and neoangiogenesis. However, little is known about the significance of atypical receptors for chemokines (ACKRs) in these tumors. The objective of the study was to present the role of chemokines and their conventional and atypical receptors in CNS tumors. Therefore, we performed a thorough search for literature concerning our investigation via the PubMed database. We describe biological functions of chemokines/chemokine receptors from various groups and their significance in carcinogenesis, cancer-related inflammation, neo-angiogenesis, tumor growth, and metastasis. Furthermore, we discuss the role of chemokines in glioma development, with particular regard to their function in the transition from low-grade to high-grade tumors and angiogenic switch. We also depict various chemokine/receptor axes, such as CXCL8-CXCR1/2, CXCL12-CXCR4, CXCL16-CXCR6, CX3CL1-CX3CR1, CCL2-CCR2, and CCL5-CCR5 of special importance in gliomas, as well as atypical chemokine receptors ACKR1-4, CCRL2, and PITPMN3. Additionally, the diagnostic significance and usefulness of the measurement of some chemokines and their receptors in the blood and cerebrospinal fluid (CSF) of glioma patients is also presented.
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Ulvmar, Maria Helena, Elin Hub, and Antal Rot. "Atypical chemokine receptors." Experimental Cell Research 317, no. 5 (March 2011): 556–68. http://dx.doi.org/10.1016/j.yexcr.2011.01.012.
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Gencer, Selin, Emiel van der Vorst, Maria Aslani, Christian Weber, Yvonne Döring, and Johan Duchene. "Atypical Chemokine Receptors in Cardiovascular Disease." Thrombosis and Haemostasis 119, no. 04 (February 4, 2019): 534–41. http://dx.doi.org/10.1055/s-0038-1676988.
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AbstractInflammation has been well recognized as one of the main drivers of atherosclerosis development and therefore cardiovascular diseases (CVDs). It has been shown that several chemokines, small 8 to 12 kDa cytokines with chemotactic properties, play a crucial role in the pathophysiology of atherosclerosis. Chemokines classically mediate their effects by binding to G-protein-coupled receptors called chemokine receptors. In addition, chemokines can also bind to atypical chemokine receptors (ACKRs). ACKRs fail to induce G-protein-dependent signalling pathways and thus subsequent cellular response, but instead are able to internalize, scavenge or transport chemokines. In this review, we will give an overview of the current knowledge about the involvement of ACKR1–4 in CVDs and especially in atherosclerosis development. In the recent years, several studies have highlighted the importance of ACKRs in CVDs, although there are still several controversies and unexplored aspects that have to be further elucidated. A better understanding of the precise role of these atypical receptors may pave the way towards novel and improved therapeutic strategies.
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Legler, Daniel F., and Marcus Thelen. "New insights in chemokine signaling." F1000Research 7 (January 23, 2018): 95. http://dx.doi.org/10.12688/f1000research.13130.1.
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Chemokine signaling is essential for coordinated cell migration in health and disease to specifically govern cell positioning in space and time. Typically, chemokines signal through heptahelical, G protein-coupled receptors to orchestrate cell migration. Notably, chemokine receptors are highly dynamic structures and signaling efficiency largely depends on the discrete contact with the ligand. Promiscuity of both chemokines and chemokine receptors, combined with biased signaling and allosteric modulation of receptor activation, guarantees a tightly controlled recruitment and positioning of individual cells within the local environment at a given time. Here, we discuss recent insights in understanding chemokine gradient formation by atypical chemokine receptors and how typical chemokine receptors can transmit distinct signals to translate guidance cues into coordinated cell locomotion in space and time.
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Gustavsson, Martin, Douglas P. Dyer, Chunxia Zhao, and Tracy M. Handel. "Kinetics of CXCL12 binding to atypical chemokine receptor 3 reveal a role for the receptor N terminus in chemokine binding." Science Signaling 12, no. 598 (September 10, 2019): eaaw3657. http://dx.doi.org/10.1126/scisignal.aaw3657.
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Chemokines bind to membrane-spanning chemokine receptors, which signal through G proteins and promote cell migration. However, atypical chemokine receptor 3 (ACKR3) does not appear to couple to G proteins, and instead of directly promoting cell migration, it regulates the extracellular concentration of chemokines that it shares with the G protein–coupled receptors (GPCRs) CXCR3 and CXCR4, thereby influencing the responses of these receptors. Understanding how these receptors bind their ligands is important for understanding these different processes. Here, we applied association and dissociation kinetic measurements coupled to β-arrestin recruitment assays to investigate ACKR3:chemokine interactions. Our results showed that CXCL12 binding is unusually slow and driven by the interplay between multiple binding epitopes. We also found that the amino terminus of the receptor played a key role in chemokine binding and activation by preventing chemokine dissociation. It was thought that chemokines initially bind receptors through interactions between the globular domain of the chemokine and the receptor amino terminus, which then guides the chemokine amino terminus into the transmembrane pocket of the receptor to initiate signaling. On the basis of our kinetic data, we propose an alternative mechanism in which the amino terminus of the chemokine initially forms interactions with the extracellular loops and transmembrane pocket of the receptor, which is followed by the receptor amino terminus wrapping around the core of the chemokine to prolong its residence time. These data provide insight into how ACKR3 competes and cooperates with canonical GPCRs in its function as a scavenger receptor.
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Pacheco, Messias Oliveira, Fernanda Agostini Rocha, Thiago Pinheiro Arrais Aloia, and Luciana Cavalheiro Marti. "Evaluation of Atypical Chemokine Receptor Expression in T Cell Subsets." Cells 11, no. 24 (December 16, 2022): 4099. http://dx.doi.org/10.3390/cells11244099.
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Chemokines are molecules that pertain to a family of small cytokines and can generate cell chemotaxis through the interaction with their receptors. Chemokines can trigger signaling via conventional G-protein-coupled receptors or through atypical chemokine receptors. Currently, four atypical chemokine receptors have been are described (ACKR1, ACKR2, ACKR3 and ACKR4). ACKRs are expressed in various cells and tissues, including T lymphocytes. These receptors’ main function is related to the internalization and degradation of chemokines, as well as to the inflammation control. However, the expression of these receptors in human T lymphocytes is unclear in the literature. The objective of this study was to evaluate the expression of ACKRs in different subpopulations of T lymphocytes. For this, peripheral blood from healthy donors was used to analyze the expression of ACKR2, ACKR3 and ACKR4 by immunophenotyping CD4, CD8 T lymphocytes and, in their subsets, naive, transition and memory. Results obtained in this study demonstrated that ACKR2, ACKR3 and ACKR4 receptors were expressed by T lymphocytes subsets in different proportions. These receptors are highly expressed in the cytoplasmic milieu of all subsets of T lymphocytes, therefore suggesting that their expression in plasma membrane is regulated after transcription, and it must be dependent on a stimulus, which was not identified in our study. Thus, regarding ACKRs function as scavenger receptors, at least for the ACKR3, this function does not impair the chemotaxis exert for their ligand compared to the typical counterpart receptor.
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Miyabe, Yoshishige, Chie Miyabe, Vinidhra Mani, Thorsten R. Mempel, and Andrew D. Luster. "Atypical complement receptor C5aR2 transports C5a to initiate neutrophil adhesion and inflammation." Science Immunology 4, no. 35 (May 10, 2019): eaav5951. http://dx.doi.org/10.1126/sciimmunol.aav5951.
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Chemoattractant-induced arrest of circulating leukocytes and their subsequent diapedesis is a fundamental component of inflammation. However, how tissue-derived chemoattractants are transported into the blood vessel lumen to induce leukocyte entry into tissue is not well understood. Here, intravital microscopy in live mice has shown that the “atypical” complement C5a receptor 2 (C5aR2) and the atypical chemokine receptor 1 (ACKR1) expressed on endothelial cells were required for the transport of C5a and CXCR2 chemokine ligands, respectively, into the vessel lumen in a murine model of immune complex–induced arthritis. Transported C5a was required to initiate C5aR1-mediated neutrophil arrest, whereas transported chemokines were required to initiate CXCR2-dependent neutrophil transdendothelial migration. These findings provide new insights into how atypical chemoattractant receptors collaborate with “classical” signaling chemoattractant receptors to control distinct steps in the recruitment of neutrophils into tissue sites of inflammation.
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Leick, Marion, Julie Catusse, and Meike Burger. "The Atypical Chemokine Receptor CRAM Mediates CCL19 Transcytosis through Endothelial Cells and Modulates CCL19 Activation of Non-Hodgkin Lymphoma B Cells." Blood 114, no. 22 (November 20, 2009): 2672. http://dx.doi.org/10.1182/blood.v114.22.2672.2672.
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Abstract Abstract 2672 Poster Board II-648 Introduction: Chemokines work as cellular recruitment molecules. Specific combinations of chemokines, receptors, and adhesion molecules determine which subgroups of leukocytes migrate and what their destinations are. Chemokine receptor expression and activation on malignant cells may be involved in the growth, survival and migration of cancer cells as well as in the tumor vascularisation. CCR7, by binding the chemokines CCL19 and CCL21, is centrally involved in B cell localisation to the secondary lymphoid organs and therefore implicated in lymphadenopathy of various non-hodgkin lymphomas (NHL). In addition to chemokine receptors that have been cloned and described, various orphan receptors with a chemokine receptor-like structure are still not characterized. Atypical, non-signaling chemokine receptors are members of a newly described class of receptors and have been implicated with chemokine clearance and influencing of other signalling receptors. They are consequently considered as potent immuno-modulators and as anti-inflammatory factors and are implicated in progression of cancer. Among these receptors, we are investigating the role of the orphan chemokine (C-C motif) receptor-like 2 (CCRL2), also known as CRAM, a receptor expressed on endothelial cells and B cells in a maturation stage dependent manner, but for which functions and ligands are poorly characterized so far. In an effort to elucidate the role of CRAM and its implication in neoplasias, we have focussed research on identification of ligands and the implication of CRAM in regulating B cell migration in samples from healthy donors and from non-Hodgkin lymphomas. Methods: We characterised the receptor's expression profile by flow cytometry in peripheral blood, bone marrow and lymph node sections of different B cell NHL and correlated it to expression levels of CCR7 and CXCR4. In addition, a screening for ligands was performed using radiolabelled binding assays. The role of CRAM was elucidated using various functional assays, internalisation and transcytosis experiments. Results: We show that CRAM is an alternative, but non-signaling receptor for the CCR7-activating chemokine CCL19. CRAM is constitutively recycling to and from the cell surface and internalizing the chemokine without degrading it. We found that the receptor is responsible for transcytosis of CCL19 through endothelial cell layers and subsequent presentation, a crucial step in homing of leukocytes to the lymph nodes. On the other hand, when expressed on B cells, CRAM interferes in CCL19 binding to CCR7. We thereby show that CRAM can act as an integrator of different signals, by binding different chemokines and controlling their activity toward surrounding ligands. Chemotaxis experiments demonstrate that CRAM is a negative modulator of CCL19 B cell recruitment. In addition, we have found increased expression in activated B cells, dendritic cells, and also in the B cell malignancies chronic lymphocytic leukemia (B-CLL) and pre-B cell acute lymphoblastic leukemia (pre-B ALL), and are currently evaluating CRAM as a possible prognostic marker in various B-NHLs. Conclusions: CRAM is a newly identified member of the silent or atypical chemokine receptor group, already known for modulating chemokine availability, together with D6, DARC and CCX-CKR. We have shown here that it contributes to lymphocyte recruitment into peripheral lymphoid tissue by presenting CCL19 on endothelium. It is also involved in CCR7 driven recruitment of B cells by regulating CCL19 availability. Expression of CRAM differs in B cell malignancies for which both CCR7 ligands, CCL19 and CCL21, have already been shown to be implicated in the development of lymphadenopathies. We therefore suggest that CRAM is an additional player and potential biomarker in determining outcome and development of disease. Disclosures: No relevant conflicts of interest to declare.
Dissertations / Theses on the topic "Atypical Chemokine Receptors"
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Tiplady, Eleanor Margaret. "Expression and modulation of atypical chemokine receptors on epithelial cells." Thesis, University of Glasgow, 2018. http://theses.gla.ac.uk/30618/.
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The immune system relies on the correct spatial and temporal positioning of cells in order to function; cells need to be able to move throughout the circulatory system to survey for pathogens, to migrate from their resident sites in tissues when they sense infection or injury to alert other cells, or to migrate to the site of damage or infection to help mobilise a response. These functions often involve chemokines, small cytokines that signal through chemokine receptors, which are G-protein coupled receptors expressed on the cell membrane. Different chemokines are regulated differentially and can be associated with certain tissues or developmental processes, meaning the suite of receptors expressed by each cell type determines which tissues it is capable of entering, and the precise location it takes up once inside the tissue. Atypical chemokine receptors are a class of chemokine receptors that do not initiate the downstream signalling pathways typical of a G-protein coupled receptor, as they do not recruit intracellular G-proteins, and generally don't induce cell migration. Instead, these receptors are thought to function mainly as chemokine scavenging receptors, internalising and destroying their ligands before rapidly recycling to the cell surface. In this way, the levels of chemokines in the body are prevented from becoming oversaturated thus dampening the ability of cells to respond to signals. ACKR3 and ACKR4 are two atypical chemokine receptors that are expressed on endothelial cells and keratinocytes in the skin. Here, I have studied their expression on cultured human lymphatic endothelial cells and keratinocytes, and modulation in response to immune stimuli on these cells using a combination of qPCR and immunofluorescent staining. These strategies revealed that ACKR3 and ACKR4 are expressed on cultured LECs and keratinocytes and may be differentially regulated by both cell types in response to inflammatory stimuli including bacterial (LPS) and viral (Unmethylated CpG DNA) signatures. Although chemokine scavenging activity could not be detected on these cells, these findings suggested a role for ACKRs 3 and 4 in the inflammatory response. Further experiments in vivo explored the expression and modulation of ACKR3/CXCR4 and ACKR4 on epithelial cells including lymphatic endothelial cells, keratinocytes and vascular endothelial cells in the spleen. Flow cytometry was used to examine tissues both at rest and after inflammation (Aldara-mediated psoriasis model, or TPA-mediated contact hypersensitivity model) and investigate the regulation of ACKR3/CXCR4 or ACKR4 in response to these stimuli. Key findings included the strong overlap and differential regulation of ACKR3 and CXCR4 in response to TPA in the infundibulum subset of keratinocytes. Additionally, lymph nodes of Ackr4-/- mice were significantly enlarged after repeated treatments with Aldara. This appeared to be due to CCL19 dysregulation, but adoptive transfer suggested that there was no defect in leukocyte homing in these mice. This suggested an as yet undetermined response to enhanced CCL19 bioavailability that did not prevent the correct migration of leukocytes to secondary lymphoid organs. Overall, these experiments suggested that ACKR3 and ACKR4 are modulated in response to several inflammatory stimuli both in vivo and in vitro, and that the modulation of homeostatic chemokines can play a role in the response to inflammatory events. This was particularly important in the context of skin inflammation, where inflammatory chemokines, CXCR4 and ACKR2 have all been implicated in severity and duration of inflammatory events, but few studies have yet described the potential contributions of ACKR3 or ACKR4.
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Benoit, Alice. "Identification du rôle de l’hypoxie dépendante de HIF-1α dans la régulation de l’expression de ACKR2 (Atypical Chemokine Receptor 2) dans le cancer." Electronic Thesis or Diss., Université de Lorraine, 2024. http://www.theses.fr/2024LORR0051.
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Les thérapies anti-cancéreuses, notamment l'immunothérapie, ont fait des progrès considérables ces dernières années ; cependant, seul un petit nombre de patients en tire un bénéfice clinique important et durable. Cela s'explique en partie par l'échec des cellules immunitaires cytotoxiques à infiltrer le microenvironnement des tumeurs. L'infiltration immunitaire dépend notamment du réseau de chimiokines, régulé en partie par les ACKRs. Le but de ce projet de thèse était d'étudier les mécanismes impliqués dans la régulation de ACKR2, qui est impliqué dans la régulation du réseau de chimiokines pro-inflammatoires. Des données in silico ont montré que les promoteurs murins et humains de ACKR2 contiennent des éléments de réponse à l'hypoxie. In vitro, les cellules de cancer colorectal, de mélanome et de cancer du sein hypoxiques surexprimaient ACKR2, ce qui n'était plus le cas pour les cellules présentant une délétion de HIF-1α. In vivo, une diminution de ACKR2 était également observée dans les tumeurs délétées en HIF 1α et associée à une hausse de CCL5 et de l'infiltration immunitaire. L'immunoprécipitation de chromatine a montré que HIF-1α se lie directement sur les motifs HRE du promoteur de ACKR2 dans les cellules de mélanomeAnti-cancer therapies, particularly immunotherapy, have made considerable progress in recent years; however, only a small number of patients derive significant and lasting clinical benefit. The incapacity of cytotoxic immune cells to infiltrate the tumor microenvironment explains in part this phenomenon. Immune infiltration depends in particular on the chemokine network, regulated in part by ACKRs. The aim of this thesis was to study the mechanisms involved in the regulation of ACKR2, which regulates the pro inflammatory chemokine network. In silico data showed that both murine and human ACKR2 promoters contain hypoxia response elements. In vitro, hypoxic colorectal, melanoma and breast cancer cells overexpressed ACKR2, which was no longer the case for cells with a deletion of HIF-1α. In vivo, ACKR2 expression was also decreased in HIF-1α-deleted tumors and associated with increased CCL5 and immune infiltration. Chromatin immunoprecipitation showed HIF-1α directly binds onto the HRE motifs of ACKR2 promoter in melanoma cells
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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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Hurson, Catherine Eileen. "Expression and function of the atypical chemokine receptor CCX-CKR." Thesis, University of Glasgow, 2011. http://theses.gla.ac.uk/2718/.
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The ability to clear infections and repair injury is dependent on the coordinated migration of immune cells, or leukocytes. These cells can directly destroy invading pathogens and also produce a variety of bioactive factors that promote pathogen clearance. Interactions between immune cells occur both at the site of inflammation and in specialised lymphoid organs throughout the body. The efficiency and specificity of these interactions relies on the production of a family of molecules called chemotactic cytokines, or chemokines, that drive leukocyte migration. Cells express specific profiles of chemokine receptors to ensure they are directed to the appropriate location to exert their immunological function. The field of chemokine biology, already complex, has been further complicated by the discovery of a subfamily of receptors, the atypical chemokine receptors. These molecules lack the ability to couple to signal transduction pathways used by the other chemokine receptors, and are proposed to act as chemokine scavengers or transport molecules. The atypical chemokine receptor CCX-CKR was discovered more than a decade ago but its function in vivo remains unclear. At the beginning of my project, information about this molecule was very limited. The murine receptor binds the CC chemokines CCL19, CCL21 and CCL25, which have well-characterised and critical roles in the development and homeostasis of the immune system as well as in the immune response to infection. Thus, identification of this new receptor, which unlike classical receptors does not induce cell migration in response to ligand binding, presented some exciting possibilities as to how these processes might be regulated in vivo. Reports describing the pattern of expression of CCX-CKR have thus far provided only limited and sometimes contradictory information. Additionally, while in vitro studies from our lab have provided some important clues as to the potential role of the receptor, published in vivo studies were, at the time of commencing this work, limited to one report describing an unvalidated EGFP reporter knock-in transgenic mouse and a conflicting online resource detailing data generated using a LacZ reporter mouse. To understand the true function of this molecule, it is critical to know where it is expressed in vivo and to explore its function on these cells. In this project I set out with the aim of identifying murine tissues and cells expressing CCX-CKR, as well as examining its potential as an in vivo scavenger of chemokine. Related to this, I hoped to uncover any impact of deletion of CCX-CKR on lymphoid tissue cellularity and/or function, both in resting and inflamed conditions. In chapter 3, I present data that identify lymphoid tissues and “barrier” tissues as sites of robustly detectable CCX-CKR mRNA expression. I describe how I have established a novel fluorescent chemokine tetramer-based protocol for the detection of CCL19 receptors, with emphasis on the application of this protocol to identify CCX-CKR activity on specific cell subsets. Using this method, I present evidence that some CD11b+ CD11c+ myeloid subsets in the inguinal lymph node exhibit CCX-CKR dependent internalisation of chemokine. I also describe attempts to fractionate tissues to identify cell populations responsible for the detected whole-tissue expression of CCX-CKR mRNA. The results described in chapter 4 provide support for the hypothesis that CCX-CKR regulates levels of its ligands in vivo, with alterations in chemokine levels in serum and inguinal lymph nodes in the absence of CCX-CKR. I also present evidence demonstrating that deletion of the receptor can influence mRNA levels of the related receptor CCR7. Following on from this, chapter 5 details my analysis of the impact of CCX-CKR on the cellularity of various lymphoid compartments. I present evidence that CCX-CKR influences lymphocyte populations in the peritoneal cavity, with both innate-like and conventional lymphocytes significantly overrepresented in this compartment. The cellularity of the inguinal lymph node, but not the spleen, is subtly altered by deletion of the receptor. Splenic leukocyte cellularity is not affected, either in number or in localisation. In chapter 6, I turn my attention to the possible role of CCX-CKR during the inflammatory response by examining various experimental parameters during a short-term model of induced cutaneous inflammation. This study shows that CCX-CKR deletion alters the cellularity of the myeloid compartment in the draining lymph node and again highlights myeloid subsets as displaying CCX-CKR dependent chemokine internalisation. Finally, I present preliminary data suggesting a protective effect of CCX-CKR deletion during a long-term model of inflammation-driven tumorigenesis. Taken together, my data provide tentative support for the theory that CCX-CKR acts as a chemokine scavenger in vivo. They further indicate that CCX-CKR is involved in regulating cellularity of various lymphoid compartments both at rest and during induced inflammation. In chapter 7 I discuss in detail the implications of my findings in the context of work published since my project began, and highlight growing evidence to suggest a role for CCX-CKR in regulating immune function.
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King, Vicky. "Assessment of the therapeutic potential of the atypical chemokine receptor, D6." Thesis, University of Glasgow, 2010. http://theses.gla.ac.uk/2165/.
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Infiltration of inflammatory cells into the tissue during the inflammatory response is beneficial to the host. Chemokines and their receptors are instrumental in this process by influencing the migration and behaviour of leukocytes in the tissue. However, prolonged inflammation is associated with many diseases. In recent years, a family of atypical receptors have emerged which do not seem to signal. One of these receptors, D6, is able to internalise and degrade 12 pro-inflammatory CC chemokines and has a role in the resolution of the inflammatory response. Here, using a murine transgenic approach, the potential therapeutic role of D6 in suppressing cutaneous inflammation in vivo has been investigated, using a well-characterised model of skin inflammation. In addition, expression of D6 in a range of inflammatory disorders has also been characterised. Transgenic mice were generated (K14D6), using an epidermis-specific transgene, in which expression of the D6 transgene was driven by the human keratin 14 promoter in epidermal keratinocytes. K14D6 mice were validated and we have shown that D6 is expressed in K14D6 but not in wild-type epidermal keratinocytes. The K14D6 transgene was shown to be functional as only K14D6 keratinocytes were able to bind CCL2 and progressively deplete extracellular CCL3. K14D6 mice can dampen down cutaneous inflammation in response to a topical application of TPA. In addition, K14D6 mice displayed reduced infiltration of epidermal T cells and mast cells compared to wild-type mice. Using a microarray approach, we examined the transcriptional consequences of non-ligated D6 and after ligand binding in primary murine keratinocytes from K14D6 and wild-type mice. Although limited conclusions could be made from the microarray data, our results suggest the possibility that non-ligated D6 in murine keratinocytes may have a negative impact on the transcription of some genes, such as chemokines. In a previous study, D6 null mice displayed a human psoriasis-like pathology after chemical induced skin inflammation, suggesting a possible involvement of D6-dysfunction as a contributing factor in the pathogenesis of psoriasis. We have investigated the possible correlation between D6 expression levels and cutaneous disease development. Analysis of skin biopsies revealed that D6 mRNA levels were 8-fold higher in uninvolved psoriatic skin compared to matching psoriatic lesional skin, atopic dermatitis and control skin. In PBMCs, there was no significant difference in D6 mRNA expression in psoriasis patients compared to control. A preliminary study examining surface D6 expression on leukocytes from control and rheumatoid arthritis patients revealed enhanced D6 expression on B cells and myeloid DCs. In this study, we have shown for the first time that increased expression of D6 in vivo can limit cutaneous inflammation, therefore providing a rationale for exploring the therapeutic potential of D6 in human inflammatory diseases. In addition, we provide evidence that D6 expression is dysregulated in inflammatory disorders further suggesting an involvement of this receptor in the pathogenesis of these diseases.
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Teoh, Pek Joo. "The role of the atypical chemokine receptor D6 in the placenta." Thesis, University of Glasgow, 2014. http://theses.gla.ac.uk/5098/.
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D6 is an atypical chemokine receptor related to CCR1-5 that binds to many inflammatory CC chemokines. Experiments using transfected cell lines have shown that upon binding to a chemokine ligand D6 does not trigger cellular signalling pathways, but rather acts to scavenge the bound ligand. It achieves this by constitutively travelling to and from the cell surface via early and recycling endosomes, internalising chemokines bound when it is at the cell surface. Over time, D6 removes a large amount of ligands from the extracellular compartment. In vivo, this scavenging activity is thought to regulate the level of CC chemokines, and thus controls inflammation locally and systemically. Lack of D6 has been shown to result in elevated amounts of bioavailable chemokines, and is associated with over exuberant inflammatory responses. In human, D6 mRNA and protein is highly expressed in trophoblast-derived gestational tissues. The expression of D6 mRNA in the placenta is by far the highest, compared to other solid tissues being studied. The importance of D6 in protecting the offspring has been demonstrated in animals. In pigs, a defect in D6 expression was discovered in placental attachment sites in endometrium from arresting fetuses. In mice, lack of D6 results in an increase in fetal loss after challenge with lipopolysaccharide (LPS) or antiphospolipid autoantibodies (aPL), and an increase in the number of abnormal pups when mouse embryos are transferred into fully allogeneic pseudo-pregnant female recipients. In view of these results suggesting a critical role for D6 in placental mediated complications, the expression and molecular function of D6 in primary human trophoblast cells were studied, as to date in vitro human studies have utilised the choriocarcinoma cell line BeWo or immortalised cell lines engineered to over-express exogenous D6. Secondly the impact of D6 deficiency on placental structure, chemokine expression and leukocyte abundance in mice was examined. Chapter 3 presents the results of experiments on primary human trophoblasts. Protocols for routine primary trophoblast isolation, purification and culture from fresh term placentas were optimised in our laboratory. D6 mRNA was detected in these primary cells. Using Western blotting, immunofluorescence and flow cytometry, D6 was shown to be present predominantly in the intracellular vesicles of the cells. Competition chemokine uptake assays, analysed by flow cytometry, showed that CCL2 was internalised by trophoblasts using D6. Competitive chemokine scavenging assays, analysed by quantitative Western blot, confirmed that D6 was functioning as a chemokine scavenger on primary human trophoblasts and that it progressively removed substantial quantities of chemokine from medium bathing the cells. This is the first set of experiments that confirms D6 is present, and functioning as a chemokine scavenger in primary human cells. Chapter 4 contains the results from the mouse experiments. Even in an unchallenged environment it was shown that, on the DBA-1 genetic background, D6 deficiency in the mother and pups leads to higher rates of stillbirth and neonatal deaths, resulting in a reduction in the number of pups weaned per litter than their WT counterparts. By gestational age E14, pup weight was significantly smaller in the D6 KO mice. Using stereological techniques, the placenta of the D6 KO mice at this gestation was found to have a smaller labyrinthine zone. The volume of the labyrinthine zone was positively correlated with pup/placenta ratio. These phenotypes could be due to a maternal or fetal effect of D6 deficiency. To ascertain the answer to this question, the experiment at E14 was extended by breeding DBA-1 females heterozygous for the deleted D6 allele (D6 HET) with D6 deficient (D6 KO) males. In this model the phenotypes of D6 KO pups and placentas could be compared with their D6 HET siblings that developed in a mother expressing some D6 (i.e. D6 HET). Although there were no differences in pup weight, placental weight and pup/placenta ratio between these two groups, stereology revealed a decrease in labyrinthine zone volume fraction in the D6 KO placentas in comparison to their D6 HET siblings. The observed fetal compromise and placental defect at E14 was not apparent at the later gestational age of E18. Luminex multiplex protein assay showed an elevated level of circulating chemokine CCL2 in the serum of D6 KO pregnant mice in comparison to their WT counterpart, so loss of chemokine regulation could be responsible for the defects observed in D6 deficient placentas. In summary, D6 deficiency results in an increase in perinatal death, a fundamental defect in placental formation (reduced labyrinthine zone) and dysregulation of circulating chemokine levels. Chapter 5 discusses the mechanisms of D6 in regulating placental formation and reproductive outcome and the novel insights that this work provided into placental D6 function. It also describes the design of future experiments to reveal the precise role of D6 in chemokine regulation and cell signalling in reproductive immunology, and discusses how D6 might contribute to pregnancy outcome in humans.
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Lucas, Beth. "Expression and function of the atypical chemokine receptor CCRL1 in the thymus." Thesis, University of Birmingham, 2015. http://etheses.bham.ac.uk//id/eprint/5971/.
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Thymus colonisation and thymocyte positioning are mediated by interactions involving CCR7 and CCR9 and their respective ligands CCL19/CCL21 and CCL25. These chemokines also interact with the atypical receptor CCRL1, which is expressed in the thymus and has recently been reported to play an important role in normal abT-cell development. Our study has mapped CCRL1 expression within the adult and embryonic thymus, and shows that CCRL1 is expressed within the thymic cortex, at the subcapsular zone, and surrounding vessels at the corticomedullary junction. We have used flow cytometry to show CCRL1 expression predominantly by cortical thymic epithelial cells, but also by a small population of medullary thymic epithelial cells and by a subset of mesenchymal cells. We show, using CCRL1 deficient mice, that CCRL1 suppresses thymocyte progenitor entry into the thymus, and influences the intrathymic positioning of double negative thymocytes. Nevertheless, we have shown that CCRL1-/- mice have no major perturbations in T- cell populations at different stages of thymic differentiation and development. Overall, this study characterises the expression of CCRL1 in key thymic microenvironments, but argues against a major role for CCRL1 in normal thymus development and function.
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Vacchini, A. "ANALYSIS OF BIASED SIGNALING IN THE CHEMOKINE SYSTEM." Doctoral thesis, Università degli Studi di Milano, 2016. http://hdl.handle.net/2434/365864.
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Chemokines constitute a family of almost 50 small secreted cytokines, recognized by about 20 different 7TM spanning G protein coupled receptors (GPCRs), that activating pertussis toxin sensitive G proteins induce cell migration. These receptor are abundantly expressed by leukocytes and, controlling cell migration, they dictate leukocyte positioning during homeostatic patrolling within peripheral tissues, their maintenance in bone marrow during maturation and in addition mediate their recruitment to inflamed tissues. Upon inflammation in fact a number of chemokines are produced or activated by inflammatory mediators and diffuse within the tissue, generating a chemical gradient along which leukocytes migrate to reach the center of inflammation to contain and remove the insulting factor. This system needs an extremely tight control, since its dysregulation has been demonstrated to be at the basis of different inflammatory diseases, auto-immunity and has also been linked to cancer development. In particular, in this thesis we focused our attention on two regulatory system: post-translational modifications of chemokines, mediated by enzymes specifically released upon inflammation also by immune cells, and on the activity of atypical chemokine receptors, a subfamily of chemokine receptors that despite high structural homology and similar binding properties compared to conventional chemokine receptors, are unable to drive chemotaxis but act instead as key regulators of the chemokine system activity. In detail we looked at the ability of these regulatory mechanisms to modulate chemokine signaling properties generating a biased signaling, an emerging feature of GPCR pharmacology that describes the ability of a given receptor to elicit different or even opposite functional activities depending on the ability of different agonists to stabilize different receptor’s active structural conformation, resulting in different phenotypes mediated by the same receptor. In the chemokine system biased signaling has already been described to occur on different receptors upon binding of their different ligands, therefore during our investigation on chemokine regulatory system signaling we maintained our focus on the ability of these systems to bias chemokine signaling properties in order to better understand how this regulation occurs.
To this point we assessed the ability of differently post-translationally modified chemokines to elicit signaling activities on different receptors by measuring in HEK293 cells their potential in inhibiting adenylyl cyclase, a proximal downstream signal of Gα inhibitory proteins activation, and in inducing β-arrestin recruitment to the receptors in energy transfer-based assays. We also compared signaling properties of an atypical chemokine receptor to the ones elicited by a conventional receptor analyzing the phosphoproteome modifications occurring constitutively and after stimulation with the same agonist.
Our results indicate that regulation of CXCL5 and CXCL8 chemokine activity by post-translational modifications is more prone to regulate chemokine activity modifying chemokine potency, rather than generating a bias in their signaling properties. Truncation of chemokine NH2-terminus increases both CXCL5 and CXCL8 activity, while citrullination of the most NH2-terminal arginine results in opposite effects on the two agonists since on CXCL8 increases chemokine potency, while it reduces CXCL5 activity. We investigated the properties of ACKR2 in recruiting β-arrestins, demonstrating that this receptor is able to associate both β-arrestin 1 and 2 in basal conditions while upon agonist stimulation preferentially increases its association with β-arrestin 1, resulting in a completely different agonist-induced outcome of proteome phosphorylation, compared to CCR5, in terms of kinetics, protein phosphorylation modifications, biological function of the regulated proteins and signal mediators activated. Taken together, these results indicate that chemokine system regulation is based not only on chemokine post-translational modifications that modulate chemokine potency, but also on the activity of structurally biased atypical chemokine receptors, as in the case of ACKR2 that interacts with different effectors and kinetics to generate distinct functional outcomes, compared to the conventional chemokine receptor CCR5.
In this thesis it has also been attempted to translate the investigation of chemokine signaling to a clinical intervention for inflammatory diseases. We assessed the modulation of CXCR1 signaling activity exerted by Reparixin, a leukocyte migration inhibitor that blocks cell recruitment to inflamed tissues, that binds to its target receptors in an allosteric binding site, without inhibiting chemokine binding to the receptor. In our assays performed on HEK293 cells we could not detect any inhibition of the signaling pathways assayed, possibly indicating that HEK293 cells are not the best model to assay the activity of this molecule, with the need to assess in this cellular model drug inhibitory activity on read-outs already evaluated in literature on other cell types.
In conclusion, we can say that observations described in this thesis allow to better understand chemokine system regulation, that occurs by biased signaling activity in the case of atypical chemokine receptors that by selected interaction with signaling mediators induce opposite biological outcomes compared to conventional chemokine receptors, while post-translational modifications regulate chemokines activity modulating their potency, rather than biasing their signaling properties.
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Shams, Kave. "The role and regulation of the atypical chemokine receptor 2 in psoriasiform inflammation." Thesis, University of Glasgow, 2017. http://theses.gla.ac.uk/8121/.
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Psoriasis is a common, debilitating systemic inflammatory disorder that is characterised by sharply demarcated, thick, erythematous scaly skin plaques. Such plaques commonly appear on skin that is subjected to repeated tensile trauma, such as elbows, knees and flexures. The mechanism by which these inflammatory lesions are spatially restricted is not known and yet knowledge of this could be of critical importance for our understanding of this disease. Chemokines are the principal regulators of leukocyte migration and play a critical role in the initiation and maintenance of inflammation. The atypical chemokine receptor ACKR2 (formerly D6) binds inflammatory CC-chemokines, but does not signal upon ligand binding; instead ACKR2 internalises and helps degrade such chemokines, after which it continues to cycle back to the cell surface. ACKR2 acts, through this mechanism, as a high-capacity scavenger of chemokines, and plays an important role in regulating inflammation. It is known that ACKR2 expression is high in unaffected skin in patients with psoriasis (remote from inflammatory plaques) and concurrently deficient in the plaques themselves. Additionally, human studies have shown that simple skin trauma in psoriasis patients causes a reduction in cutaneous ACKR2 expression at the site of trauma. However, the functional significance and the molecular mechanism by which it occurs are not understood. This thesis explored the role of ACKR2 in the spatial restriction of psoriasiform inflammation and the molecular mechanisms for its differential regulation. Through the use of disease relevant mouse models, primary human cell cultures and novel cell migration assays, the results presented here show that localised psoriasiform inflammation upregulates ACKR2 in remote tissues through the systemic release of cytokines. This remotely upregulated ACKR2 expression protects tissues from the further spread of inflammation. This protective effect is mediated by stromally expressed ACKR2 that acts to control inflammatory T-cell positioning within the skin. Tensile trauma of keratinocytes however, acted to reduce ACKR2 expression in the context of inflammation, which in turn provides a novel mechanism for the well-characterised phenomenon that occurs in psoriasis (and a range of skin condition) termed ‘koebnerisation’. Koebnerisation refers to the phenomenon by which relatively simple skin trauma induces the development of disease-specific skin lesions. Furthermore, this thesis defines novel disease-relevant regulators of ACKR2 expression. In silico analyses identified psoriasis-associated microRNAs that bound to the 3’-UTR of ACKR2, and reduced its expression at transcriptional and protein level. Importantly, trauma of keratinocytes induced ACKR2 downregulation concurrent with a substantial and significant increase in the expression of the identified ACKR2 targeting microRNAs. Together, this thesis defines a novel mechanism by which ACKR2-mediated regulation of chemokine function, cutaneous trauma, microRNAs and systemic cytokines, co-ordinately modulate the predisposition of remote tissue sites to the development of new lesions. Importantly, the results presented here have profound implications for how spatial restriction is imposed on inflammation. The data also highlight therapeutic ACKR2 induction as a plausible novel strategy for the limitation and treatment of psoriasiform- and potentially other forms of inflammation.
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Korniejewska, Anna. "Characterisation of the chemokine receptor CXCR3 and its atypical variants in human T lymphocytes." Thesis, University of Bath, 2009. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.518106.
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The chemokine receptor CXCR3 and its agonists CXCL9/Mig, CXCL10/IP-10 and CXCL11/I-TAC are involved in a variety of inflammatory disorders including multiple sclerosis, rheumatoid arthritis, psoriasis and sarcoidosis. CXCL11 has also been reported to bind to an additional receptor, namely CXCR7, which also interacts with CXCL12. Two alternatively spliced variants of the human CXCR3 receptor have been described, namely CXCR3-B and CXCR3-alt. The human CXCR3-B has been found to bind CXCL9, CXCL10, CXCL11 as well as an additional agonist CXCL4/PF4. In contrast, CXCR3-alt only binds CXCL11. This work demonstrates that CXCL4 like the original CXCR3 agonists is capable of inducing biochemical signalling, namely intra-cellular calcium elevation, and activation of p44/p42 MAPK and PI3K/Akt pathways in activated human T lymphocytes. Phosphorylation of p44/p42 MAPK and Akt was inhibited by pertussis toxin, suggesting coupling to Gi protein. In contrast CXCR3 antagonists blocked CXCR3 agonists but not CXCL4-mediated responses. Surprisingly, stimulation of T cells with CXCL4 failed to elicit migratory responses of these cells and did not lead to loss of surface CXCR3 expression. Collectively our evidence shows that although CXCL4 is coupled to downstream biochemical machinery, its function in T cells is distinct from the function of CXCR3 agonists. The work presented in this thesis also indicates that despite considerably lower surface expression in comparison to the full length CXCR3, CXCR3-B and CXCR3-alt transduce biochemical signals in response to CXCL11 in transfected cells. According to previous reports the role of CXCR7 in signalling and chemotaxis in T cells could not be detected. In T cells and transfected cells system CXCR7 was localised at the plasma membrane and was efficiently internalized in response to CXCL11 and CXCL12. Studies of the involvement of methylation in T cell chemotaxis suggest that this modification may be required in this process as it was partially inhibited by methylation inhibitor- MTA. Moreover T cell co-stimulation caused increased levels of arginine mono-methylated proteins suggesting the importance of methylation in T lymphocyte signalling.
Books on the topic "Atypical Chemokine Receptors"
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Hughes, Jeremy. Proteinuria as a direct cause of progression. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0137.
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Proximal tubular cells reabsorb any filtered proteins during health via cell surface receptors such as megalin and cubulin so that very low levels of protein are present in the excreted urine. Significant proteinuria is a common finding in patients with many renal diseases. Proteinuria is a marker of glomerular damage and podocyte loss and injury in particular. The degree of proteinuria at presentation or during the course of the disease correlates with long-term outcome in many renal diseases. Proteinuria per se may be nephrotoxic and thus directly relevant to the progression of renal disease rather than simply acting as a marker of the severity of glomerular injury and podocytes loss. Seminal studies used the atypical renal anatomy of the axolotl to instill proteins directly into the tubular lumen without requiring passage through the glomerulus. This indicated that tubular protein could be cytotoxic and induce interstitial inflammation and fibrosis in the peritubular region. Cell culture studies demonstrate that exposure to proteins results in proximal tubular cell activation and the production of pro-inflammatory and pro-fibrotic mediators. Proximal tubular cell death occurred in some studies reinforcing the potential of protein to exert cytotoxic effects via oxidative stress or endoplasmic reticulum stress. Analysis of renal biopsy material from both experimental studies using models of proteinuric disease or patients with various proteinuric diseases provided evidence of activation of transcription factors and production of chemokines and pro-inflammatory mediators by proximal tubular cells. These data strongly suggest that although proteinuria is the result of glomerular disease it also represents an important cause of progression in patients with chronic kidney disease associated with proteinuria.
Book chapters on the topic "Atypical Chemokine Receptors"
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Singh, Mark D., Robert J. B. Nibbs, and Gerard J. Graham. "The Atypical Chemokine Receptors." In Methods and Principles in Medicinal Chemistry, 67–83. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2011. http://dx.doi.org/10.1002/9783527631995.ch4.
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Bonecchi, Raffaella, Matteo Massara, and Massimo Locati. "Atypical Chemokine Receptors." In Encyclopedia of Immunobiology, 579–85. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-12-374279-7.10009-8.
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Werth, Kathrin, and Reinhold Förster. "Active Shaping of Chemokine Gradients by Atypical Chemokine Receptors." In Methods in Enzymology, 293–308. Elsevier, 2016. http://dx.doi.org/10.1016/bs.mie.2015.09.008.
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Borroni, Elena, Cinzia Cancellieri, Massimo Locati, and Raffaella Bonecchi. "Dissecting Trafficking and Signaling of Atypical Chemokine Receptors." In Methods in Enzymology, 151–68. Elsevier, 2013. http://dx.doi.org/10.1016/b978-0-12-391862-8.00008-9.
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Lokeshwar, Bal L., Georgios Kallifatidis, and James J. Hoy. "Atypical chemokine receptors in tumor cell growth and metastasis." In Advances in Cancer Research, 1–27. Elsevier, 2020. http://dx.doi.org/10.1016/bs.acr.2019.12.002.
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Luís, Rafael, Giulia D’Uonnolo, Christie B. Palmer, Max Meyrath, Tomasz Uchański, May Wantz, Bernard Rogister, Bassam Janji, Andy Chevigné, and Martyna Szpakowska. "Nanoluciferase-based methods to monitor activation, modulation and trafficking of atypical chemokine receptors." In Methods in Cell Biology. Elsevier, 2022. http://dx.doi.org/10.1016/bs.mcb.2022.03.002.
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Sjöberg, Elin, Max Meyrath, Andy Chevigné, Arne Östman, Martin Augsten, and Martyna Szpakowska. "The diverse and complex roles of atypical chemokine receptors in cancer: From molecular biology to clinical relevance and therapy." In Advances in Cancer Research, 99–138. Elsevier, 2020. http://dx.doi.org/10.1016/bs.acr.2019.12.001.
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Kleist, Andrew B., Francis Peterson, Robert C. Tyler, Martin Gustavsson, Tracy M. Handel, and Brian F. Volkman. "Solution NMR spectroscopy of GPCRs: Residue-specific labeling strategies with a focus on 13C-methyl methionine labeling of the atypical chemokine receptor ACKR3." In Methods in Cell Biology, 259–88. Elsevier, 2019. http://dx.doi.org/10.1016/bs.mcb.2018.09.004.
Full textConference papers on the topic "Atypical Chemokine Receptors"
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Jenkins, Brittany D., Rupali Hire, Elizabeth Howerth, Michele Monteil, Rachel Martini, and Melissa B. Davis. "Abstract 953: Atypical chemokine receptor 1 (ACKR1/DARC) expressing tumors are associated with distinct recruitment of immune cells and increased pro-inflammatory chemokines." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-953.
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Jenkins, Brittany D., Rachel N. Martini, Rupali Hire, Michele A. Monteil, and Melissa B. Davis. "Abstract B39: Distinct recruitment of tumor-associated immune cells correlates with increased pro-malignant chemokines in tumors expressing epithelial Atypical Chemokine Receptor 1 (ACKR1/DARC)." In Abstracts: Ninth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; September 25-28, 2016; Fort Lauderdale, FL. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7755.disp16-b39.
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Salazar, Nicole, Daniel Muñoz, and Bal L. Lokeshwar. "Abstract C210: Atypical chemokine receptor 3/CXCR7 and EGFR interact to control breast cancer growth." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-c210.
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Jenkins, Brittany D., Rachel N. Martini, Inasia Brown, and Melissa B. Davis. "Abstract 5071: The functional relevance of Atypical Chemokine Receptor 1 (ACKR1/DARC) genetic isoforms in breast cancer." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-5071.
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Jenkins, Brittany D., Rachel Martini, Kevin Gardner, Michele Monteil, Dorrah Deeb, Lisa Newman, and Melissa Davis. "Abstract 4565: The functional role of atypical chemokine receptor 1 in immune cell regulation of breast cancer." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-4565.
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Jenkins, Brittany D., Rachel Martini, Kevin Gardner, Michele Monteil, Dorrah Deeb, Lisa Newman, and Melissa Davis. "Abstract 4565: The functional role of atypical chemokine receptor 1 in immune cell regulation of breast cancer." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-4565.
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Kim, Nayoung, Seung-Woo Baek, Hyewon Ryu, Yoon Seok Choi, Ik Chan Song, Hwan Jung Yun, Deog Yeon Jo, Samyong Kim, and Hyo Jin Lee. "Abstract 3947: Atypical chemokine receptor ACKR3 expression is associated with aggressive behavior and poor prognosis in gastric cancer." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-3947.
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Jenkins, BD, RN Martini, R. Hire, MA Monteil, and MB Davis. "Abstract P6-01-11: Distinct recruitment of tumor-associated immune cells correlates with increased pro-malignant chemokines in tumors expressing epithelial atypical chemokine receptor 1 (ACKR1/DARC), indicating a unique tumor microenvironment." In Abstracts: 2016 San Antonio Breast Cancer Symposium; December 6-10, 2016; San Antonio, Texas. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.sabcs16-p6-01-11.
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